INTRODUÇÃO. A ingestão aguda de 500 ml de água pode elevar a pressão arterial de forma expressiva em indivíduos com disfunção autonômica, mas parece não afetar os níveis pressóricos de indivíduos jovens saudáveis. Na hipertensão arterial sistêmica podem ocorrer alterações na modulação autonômica e, em ratos hipertensos, há evidências de que a ingestão de água seja capaz de promover aumento da pressão arterial. Entretanto, em seres humanos hipertensos, os efeitos da ingestão aguda de água ainda não são conhecidos. OBJETIVOS. Avaliar os efeitos hemodinâmicos e autonômicos da ingestão aguda de água em indivíduos portadores de hipertensão arterial sistêmica, bem como investigar os mecanismos fisiológicos envolvidos na resposta pressora. MÉTODOS. Participaram do estudo 8 indivíduos portadores de hipertensão arterial sistêmica leve (idade = 42,5±7,8 anos; índice de massa corporal= 27,1±3,4 kg/cm2) e 10 indivíduos normotensos (idade = 37,3±7,5 anos; índice de massa corporal = 25,8±3,2 kg/cm2), os quais foram submetidos à ingestão de 500 ml de água após repouso na posição supina por 30 minutos. Foram avaliadas a pressão arterial (Finapress, Ohmeda), a freqüência cardíaca, o fluxo sangüíneo do antebraço, a resistência vascular do antebraço e a atividade nervosa simpática muscular no basal e aos 10, 20 e 30 minutos após a ingestão de água. Amostras sangüíneas venosas foram coletadas no basal e aos 10 e 30 minutos após a ingestão de água, para calcular as mudanças no volume plasmático. A variabilidade da pressão arterial sistólica e da freqüência cardíaca foi avaliada por análise espectral, utilizando-se a Transformação Rápida de Fourier. RESULTADOS. A ingestão de água resultou em significativo aumento máximo das pressões arteriais sistólica (Hipertensos = 19±7 mmHg; Normotensos = 17±7 mmHg, p = 0,001) e diastólica (Hipertensos = 14±4 mmHg; Normotensos = 14±5 mmHg, p = 0,001) nos indivíduos hipertensos e normotensos. Ambos os grupos também apresentaram significativa elevação máxima da resistência vascular no antebraço (Hipertensos = 19±11 unidades; Normotensos = 20±13 unidades, p = 0,001) e da atividade nervosa simpática muscular (Hipertensos = 8±2 disparos/min; Normotensos = 8±4 disparos/min, p = 0,001). RESULTADOS. Após a ingestão de água, houve redução da freqüência cardíaca (Hipertensos = - 5,6±2,1 bat/min; Normotensos = - 5,4±7,3 bat/min, p = 0,002), do fluxo sangüíneo no antebraço (Hipertensos = - 0,5±0,4 ml/min/100 ml tecidual; Normotensos = - 0,7±0,6 ml/min/100 ml tecidual, p = 0,001) e do volume plasmático (Hipertensos = - 0,8±0,8 %; Normotensos = - 1,0±0,9%, p = 0,002) nos indivíduos hipertensos e normotensos. A variabilidade da freqüência cardíaca e da pressão arterial sistólica não foi alterada pela ingestão de água. CONCLUSÃO. A ingestão aguda de água eleva similarmente as pressões arteriais sistólica e diastólica de indivíduos hipertensos leves e normotensos, provavelmente por aumento da resistência vascular periférica, secundário à ativação simpática. / Introduction. An acute water ingestion of 500 ml may significantly increase blood pressure in individuals with autonomic dysfunction. However, it doesn’t seem to influence the pressure levels of young, healthy subjects. When a systemic arterial hypertension is present, alterations can occur in the autonomic modulation mechanism, and there is scientific evidence that acute water drinking is responsible for increases in the arterial blood pressure of laboratory rats with hypertension. However, in human subjects with hypertension, the effects of an acute water ingestion are not yet well known. Objectives. The current study aims to evaluate haemodynamics and autonomic response to acute water ingestion in human subjects that have systemic arterial hypertension, as well as to study the physiological mechanisms underlying in the pressure elevation phenomena. Method. The human subjects that participated were divided up into two study groups. The first group of eight subjects, had been diagnosed with stage I systemic hypertension (ages = 42.5±7.8 years; with a body mass index = 27.1±3.4 kg/cm2), and the second group consisted of 10 subjects that had normal pressure readings (ages = 37.3±7.5 years; with a body mass index equivalent to 25.8±3.2 kg/cm2). All participants had drunk 500ml of water, after resting for 30 minutes in the supine position. The following parameters were studied: arterial blood pressure (Finapress, Ohmeda), heart rate, forearm blood flow, forearm vascular resistance and basal muscle sympathetic nerve activity after 10, 20, and 30 minutes, immediately following the acute water ingestion. Venous blood samples were collected during the basal period of 10 and 30 minutes after water drinking, in order to calculate plasmatic volume changes. Systolic pressure and heart rate variability were evaluated by spectral analysis, utilizing the Fast Fourier Transform. Results. There was a significant maximum increase in systolic and diastolic arterial pressure, in both, hypertensive and normotensive human subjects, as a direct consequence of acute water ingestion. Systolic pressure increase was of 19±7 mmHg, in hypertensive subjects; while the same pressure increase was of 17±7 mmHg, for normotensive subjects, (p = 0.001). Similarly, the diastolic pressure increase in hypertensive subjects had an equivalent to 14±4 mmHg, and in normotensive subjects showed an increase equivalent to 14±5 mmHg, (p = 0.001). Similarly, the diastolic pressure increase in hypertensive subjects had an equivalent to 14±4 mmHg, and in normotensive subjects showed an increase equivalent to 14±5 mmHg, (p = 0.001). Also, both groups presented a significant maximum increase in forearm vascular resistance (Hypertensive = 19±11 units; normotensive = 20±13 units, p = 0.001) and in muscle sympathetic nerve activity (Hypertensive = 8±2 bursts/min, normotensive = 8±4 bursts/min, p = 0.001). After acute water ingestion, both, hypertensive and normotensive human subjects showed a decreased heart rate, forearm blood flow, and plasmatic volume. The heart rate decrease in hypertensive subjects was equal to - 5.6±2.1 beats/min; and for normotensive subjects was = - 5.4±7.3 beats/min, (p = 0.002), the forearm blood flow decrease in hypertensive subjects was = - 0.5±0.4 ml/min/100 ml tissue, and in normotensive subjects was = - 0.7±0.6 ml/min/100 ml tissue, (p = 0.001), and the plasmatic volume drop in hypertensive subjects was = - 0.8±0.8 %; and for normotensive subjects was = - 1.0±0.9%, (p = 0.002). Heart rate and systolic arterial pressure variability were not altered by acute water ingestion. CONCLUSION. An acute water ingestion equally increases systolic and diastolic arterial pressure in human subjects with stage I hypertension, as well as those normotensive ones, probably by increasing peripheral vascular resistance, which is secondary to sympathetic activity.

INTRODUÇÃO. A ingestão aguda de 500 ml de água pode elevar a pressão arterial de forma expressiva em indivíduos com disfunção autonômica, mas parece não afetar os níveis pressóricos de indivíduos jovens saudáveis. Na hipertensão arterial sistêmica podem ocorrer alterações na modulação autonômica e, em ratos hipertensos, há evidências de que a ingestão de água seja capaz de promover aumento da pressão arterial. Entretanto, em seres humanos hipertensos, os efeitos da ingestão aguda de água ainda não são conhecidos. OBJETIVOS. Avaliar os efeitos hemodinâmicos e autonômicos da ingestão aguda de água em indivíduos portadores de hipertensão arterial sistêmica, bem como investigar os mecanismos fisiológicos envolvidos na resposta pressora. MÉTODOS. Participaram do estudo 8 indivíduos portadores de hipertensão arterial sistêmica leve (idade = 42,5±7,8 anos; índice de massa corporal= 27,1±3,4 kg/cm2) e 10 indivíduos normotensos (idade = 37,3±7,5 anos; índice de massa corporal = 25,8±3,2 kg/cm2), os quais foram submetidos à ingestão de 500 ml de água após repouso na posição supina por 30 minutos. Foram avaliadas a pressão arterial (Finapress, Ohmeda), a freqüência cardíaca, o fluxo sangüíneo do antebraço, a resistência vascular do antebraço e a atividade nervosa simpática muscular no basal e aos 10, 20 e 30 minutos após a ingestão de água. Amostras sangüíneas venosas foram coletadas no basal e aos 10 e 30 minutos após a ingestão de água, para calcular as mudanças no volume plasmático. A variabilidade da pressão arterial sistólica e da freqüência cardíaca foi avaliada por análise espectral, utilizando-se a Transformação Rápida de Fourier. RESULTADOS. A ingestão de água resultou em significativo aumento máximo das pressões arteriais sistólica (Hipertensos = 19±7 mmHg; Normotensos = 17±7 mmHg, p = 0,001) e diastólica (Hipertensos = 14±4 mmHg; Normotensos = 14±5 mmHg, p = 0,001) nos indivíduos hipertensos e normotensos. Ambos os grupos também apresentaram significativa elevação máxima da resistência vascular no antebraço (Hipertensos = 19±11 unidades; Normotensos = 20±13 unidades, p = 0,001) e da atividade nervosa simpática muscular (Hipertensos = 8±2 disparos/min; Normotensos = 8±4 disparos/min, p = 0,001). RESULTADOS. Após a ingestão de água, houve redução da freqüência cardíaca (Hipertensos = - 5,6±2,1 bat/min; Normotensos = - 5,4±7,3 bat/min, p = 0,002), do fluxo sangüíneo no antebraço (Hipertensos = - 0,5±0,4 ml/min/100 ml tecidual; Normotensos = - 0,7±0,6 ml/min/100 ml tecidual, p = 0,001) e do volume plasmático (Hipertensos = - 0,8±0,8 %; Normotensos = - 1,0±0,9%, p = 0,002) nos indivíduos hipertensos e normotensos. A variabilidade da freqüência cardíaca e da pressão arterial sistólica não foi alterada pela ingestão de água. CONCLUSÃO. A ingestão aguda de água eleva similarmente as pressões arteriais sistólica e diastólica de indivíduos hipertensos leves e normotensos, provavelmente por aumento da resistência vascular periférica, secundário à ativação simpática. / Introduction. An acute water ingestion of 500 ml may significantly increase blood pressure in individuals with autonomic dysfunction. However, it doesn’t seem to influence the pressure levels of young, healthy subjects. When a systemic arterial hypertension is present, alterations can occur in the autonomic modulation mechanism, and there is scientific evidence that acute water drinking is responsible for increases in the arterial blood pressure of laboratory rats with hypertension. However, in human subjects with hypertension, the effects of an acute water ingestion are not yet well known. Objectives. The current study aims to evaluate haemodynamics and autonomic response to acute water ingestion in human subjects that have systemic arterial hypertension, as well as to study the physiological mechanisms underlying in the pressure elevation phenomena. Method. The human subjects that participated were divided up into two study groups. The first group of eight subjects, had been diagnosed with stage I systemic hypertension (ages = 42.5±7.8 years; with a body mass index = 27.1±3.4 kg/cm2), and the second group consisted of 10 subjects that had normal pressure readings (ages = 37.3±7.5 years; with a body mass index equivalent to 25.8±3.2 kg/cm2). All participants had drunk 500ml of water, after resting for 30 minutes in the supine position. The following parameters were studied: arterial blood pressure (Finapress, Ohmeda), heart rate, forearm blood flow, forearm vascular resistance and basal muscle sympathetic nerve activity after 10, 20, and 30 minutes, immediately following the acute water ingestion. Venous blood samples were collected during the basal period of 10 and 30 minutes after water drinking, in order to calculate plasmatic volume changes. Systolic pressure and heart rate variability were evaluated by spectral analysis, utilizing the Fast Fourier Transform. Results. There was a significant maximum increase in systolic and diastolic arterial pressure, in both, hypertensive and normotensive human subjects, as a direct consequence of acute water ingestion. Systolic pressure increase was of 19±7 mmHg, in hypertensive subjects; while the same pressure increase was of 17±7 mmHg, for normotensive subjects, (p = 0.001). Similarly, the diastolic pressure increase in hypertensive subjects had an equivalent to 14±4 mmHg, and in normotensive subjects showed an increase equivalent to 14±5 mmHg, (p = 0.001). Similarly, the diastolic pressure increase in hypertensive subjects had an equivalent to 14±4 mmHg, and in normotensive subjects showed an increase equivalent to 14±5 mmHg, (p = 0.001). Also, both groups presented a significant maximum increase in forearm vascular resistance (Hypertensive = 19±11 units; normotensive = 20±13 units, p = 0.001) and in muscle sympathetic nerve activity (Hypertensive = 8±2 bursts/min, normotensive = 8±4 bursts/min, p = 0.001). After acute water ingestion, both, hypertensive and normotensive human subjects showed a decreased heart rate, forearm blood flow, and plasmatic volume. The heart rate decrease in hypertensive subjects was equal to - 5.6±2.1 beats/min; and for normotensive subjects was = - 5.4±7.3 beats/min, (p = 0.002), the forearm blood flow decrease in hypertensive subjects was = - 0.5±0.4 ml/min/100 ml tissue, and in normotensive subjects was = - 0.7±0.6 ml/min/100 ml tissue, (p = 0.001), and the plasmatic volume drop in hypertensive subjects was = - 0.8±0.8 %; and for normotensive subjects was = - 1.0±0.9%, (p = 0.002). Heart rate and systolic arterial pressure variability were not altered by acute water ingestion. CONCLUSION. An acute water ingestion equally increases systolic and diastolic arterial pressure in human subjects with stage I hypertension, as well as those normotensive ones, probably by increasing peripheral vascular resistance, which is secondary to sympathetic activity.

INTRODUÇÃO. A ingestão aguda de 500 ml de água pode elevar a pressão arterial de forma expressiva em indivíduos com disfunção autonômica, mas parece não afetar os níveis pressóricos de indivíduos jovens saudáveis. Na hipertensão arterial sistêmica podem ocorrer alterações na modulação autonômica e, em ratos hipertensos, há evidências de que a ingestão de água seja capaz de promover aumento da pressão arterial. Entretanto, em seres humanos hipertensos, os efeitos da ingestão aguda de água ainda não são conhecidos. OBJETIVOS. Avaliar os efeitos hemodinâmicos e autonômicos da ingestão aguda de água em indivíduos portadores de hipertensão arterial sistêmica, bem como investigar os mecanismos fisiológicos envolvidos na resposta pressora. MÉTODOS. Participaram do estudo 8 indivíduos portadores de hipertensão arterial sistêmica leve (idade = 42,5±7,8 anos; índice de massa corporal= 27,1±3,4 kg/cm2) e 10 indivíduos normotensos (idade = 37,3±7,5 anos; índice de massa corporal = 25,8±3,2 kg/cm2), os quais foram submetidos à ingestão de 500 ml de água após repouso na posição supina por 30 minutos. Foram avaliadas a pressão arterial (Finapress, Ohmeda), a freqüência cardíaca, o fluxo sangüíneo do antebraço, a resistência vascular do antebraço e a atividade nervosa simpática muscular no basal e aos 10, 20 e 30 minutos após a ingestão de água. Amostras sangüíneas venosas foram coletadas no basal e aos 10 e 30 minutos após a ingestão de água, para calcular as mudanças no volume plasmático. A variabilidade da pressão arterial sistólica e da freqüência cardíaca foi avaliada por análise espectral, utilizando-se a Transformação Rápida de Fourier. RESULTADOS. A ingestão de água resultou em significativo aumento máximo das pressões arteriais sistólica (Hipertensos = 19±7 mmHg; Normotensos = 17±7 mmHg, p = 0,001) e diastólica (Hipertensos = 14±4 mmHg; Normotensos = 14±5 mmHg, p = 0,001) nos indivíduos hipertensos e normotensos. Ambos os grupos também apresentaram significativa elevação máxima da resistência vascular no antebraço (Hipertensos = 19±11 unidades; Normotensos = 20±13 unidades, p = 0,001) e da atividade nervosa simpática muscular (Hipertensos = 8±2 disparos/min; Normotensos = 8±4 disparos/min, p = 0,001). RESULTADOS. Após a ingestão de água, houve redução da freqüência cardíaca (Hipertensos = - 5,6±2,1 bat/min; Normotensos = - 5,4±7,3 bat/min, p = 0,002), do fluxo sangüíneo no antebraço (Hipertensos = - 0,5±0,4 ml/min/100 ml tecidual; Normotensos = - 0,7±0,6 ml/min/100 ml tecidual, p = 0,001) e do volume plasmático (Hipertensos = - 0,8±0,8 %; Normotensos = - 1,0±0,9%, p = 0,002) nos indivíduos hipertensos e normotensos. A variabilidade da freqüência cardíaca e da pressão arterial sistólica não foi alterada pela ingestão de água. CONCLUSÃO. A ingestão aguda de água eleva similarmente as pressões arteriais sistólica e diastólica de indivíduos hipertensos leves e normotensos, provavelmente por aumento da resistência vascular periférica, secundário à ativação simpática. / Introduction. An acute water ingestion of 500 ml may significantly increase blood pressure in individuals with autonomic dysfunction. However, it doesn’t seem to influence the pressure levels of young, healthy subjects. When a systemic arterial hypertension is present, alterations can occur in the autonomic modulation mechanism, and there is scientific evidence that acute water drinking is responsible for increases in the arterial blood pressure of laboratory rats with hypertension. However, in human subjects with hypertension, the effects of an acute water ingestion are not yet well known. Objectives. The current study aims to evaluate haemodynamics and autonomic response to acute water ingestion in human subjects that have systemic arterial hypertension, as well as to study the physiological mechanisms underlying in the pressure elevation phenomena. Method. The human subjects that participated were divided up into two study groups. The first group of eight subjects, had been diagnosed with stage I systemic hypertension (ages = 42.5±7.8 years; with a body mass index = 27.1±3.4 kg/cm2), and the second group consisted of 10 subjects that had normal pressure readings (ages = 37.3±7.5 years; with a body mass index equivalent to 25.8±3.2 kg/cm2). All participants had drunk 500ml of water, after resting for 30 minutes in the supine position. The following parameters were studied: arterial blood pressure (Finapress, Ohmeda), heart rate, forearm blood flow, forearm vascular resistance and basal muscle sympathetic nerve activity after 10, 20, and 30 minutes, immediately following the acute water ingestion. Venous blood samples were collected during the basal period of 10 and 30 minutes after water drinking, in order to calculate plasmatic volume changes. Systolic pressure and heart rate variability were evaluated by spectral analysis, utilizing the Fast Fourier Transform. Results. There was a significant maximum increase in systolic and diastolic arterial pressure, in both, hypertensive and normotensive human subjects, as a direct consequence of acute water ingestion. Systolic pressure increase was of 19±7 mmHg, in hypertensive subjects; while the same pressure increase was of 17±7 mmHg, for normotensive subjects, (p = 0.001). Similarly, the diastolic pressure increase in hypertensive subjects had an equivalent to 14±4 mmHg, and in normotensive subjects showed an increase equivalent to 14±5 mmHg, (p = 0.001). Similarly, the diastolic pressure increase in hypertensive subjects had an equivalent to 14±4 mmHg, and in normotensive subjects showed an increase equivalent to 14±5 mmHg, (p = 0.001). Also, both groups presented a significant maximum increase in forearm vascular resistance (Hypertensive = 19±11 units; normotensive = 20±13 units, p = 0.001) and in muscle sympathetic nerve activity (Hypertensive = 8±2 bursts/min, normotensive = 8±4 bursts/min, p = 0.001). After acute water ingestion, both, hypertensive and normotensive human subjects showed a decreased heart rate, forearm blood flow, and plasmatic volume. The heart rate decrease in hypertensive subjects was equal to - 5.6±2.1 beats/min; and for normotensive subjects was = - 5.4±7.3 beats/min, (p = 0.002), the forearm blood flow decrease in hypertensive subjects was = - 0.5±0.4 ml/min/100 ml tissue, and in normotensive subjects was = - 0.7±0.6 ml/min/100 ml tissue, (p = 0.001), and the plasmatic volume drop in hypertensive subjects was = - 0.8±0.8 %; and for normotensive subjects was = - 1.0±0.9%, (p = 0.002). Heart rate and systolic arterial pressure variability were not altered by acute water ingestion. CONCLUSION. An acute water ingestion equally increases systolic and diastolic arterial pressure in human subjects with stage I hypertension, as well as those normotensive ones, probably by increasing peripheral vascular resistance, which is secondary to sympathetic activity.