Source: Dissertation Abstracts International, Volume: 35-02, Section: B, page: 0670. / Thesis (Ph.D.)--The Florida State University, 1973.

To examine the effects of walking duration on excess post exercise oxygen consumption (EPOC), recovery substrate availability and fuel utilization, nine overfat (38.5 $\pm$ 2.4%) females completed treadmill walking sessions of 30, 45, 60, 75 and 90 minutes. Oxygen consumption (VO$\sb2$) and respiratory exchange ratio (RER) were continuously monitored by open circuit spirometry for 30 minutes before (rest) and 60 minutes following (recovery) each walking session. Resting and one-hour recovery venous blood was assayed for free fatty acid (FFA) and glycerol concentrations. Repeated measures ANOVAs were utilized for data analysis with Newman-Keuls' post-hoc employed to locate significant differences (p $\leq$ 0.05) between means. / Walking significantly elevated recovery VO$\sb2$ by 9.7%. Despite a non-significant walking duration effect, VO$\sb2$ at one hour of recovery following 30, 45, 60, 75 and 90 minutes of walking was 0.5%, 10.0%, 9.5%, 10.0% and 19.0% higher than pre-exercise rest. EPOC following 30 minutes of walking was significantly shorter in duration (minutes) and smaller in magnitude (net O$\sb2$ consumed) than for all other walking durations. Magnitude of EPOC was also significantly smaller for the 45 than the 90 minute walk. / Recovery concentrations of FFA were significantly elevated above rest following walking durations of 60, 75 and 90 minutes, while differences in rest and recovery glycerol concentrations were not significant. Respiratory exchange ratios at one-hour of recovery following both the 75 and 90 minute walks were significantly lower than respective pre-exercise resting RERs and significantly lower than recovery RERs following 30 and 45 minutes of walking. One-hour post-exercise, utilization of fat was elevated above rest by 5.4% (30 minute walk), 6.4% (45 minute walk), 9.4% (60 minute walk), 15.9% (75 minute walk) and 16.8% (90 minute walk). / A minimum walking duration of 45 minutes is required for sedentary overweight females before significant increases in recovery oxygen consumption and fat utilization occur. Recovery rates of oxygen consumption and fat utilization are further optimized as walking duration is extended to 90 minutes. Recommendations and statements concerning recovery and weight loss benefits of walking should consider these duration effects. / Source: Dissertation Abstracts International, Volume: 52-03, Section: B, page: 1273. / Major Professor: Robert J. Moffatt. / Thesis (Ph.D.)--The Florida State University, 1991.

Este trabalho consiste na realização experimental de uma Curva de Resposta de Fases (PRC) de ritmos biológicos infradianos observados em insetos cavernícolas da espécie Folsomia candida. Sendo os insetos cegos, utilizamos pulsos de temperatura para provocar os deslocamentos de fase. Obtivemos PRCs com apenas atrasos, com a característica topológica do Tipo 1, para as três durações diferentes dos pulsos utilizados. Essa característica difere das típicas respostas observadas nos osciladores do tipo ciclo-limite, os quais são associadas à maioria dos ritmos biológicos. A dimensão de um oscilador determina quais os tipo de PRCs que o sistema pode apresentar, quando sujeito a perturbações, em suas diferentes fases. Relógios simples são associados a ciclos constituídos por uma sequência discreta de eventos encadeados, estando cada evento dependente do término do anterior, para se iniciar. Esses são sistemas unidimensionais, diferindo dos ciclos-limites pela impossibilidade de apresentar PRCs do Tipo 0 e singularidades de fase. Associamos um modelo de relógios simples para os ritmos infradianos estudados, baseados nas características observadas nas PRCs e por estar de acordo com as bases fisiológicas dos mesmos. / In this work, we constructed Phase Resetting Curves (PRC) of the infradian biological rhythms of the cave insects Folsomia candida. We used temperature pulses to reset the phases of these rhythms, since the insects are blind. We obtained PRCs with delays only, of the topological Type 1, for the three different pulse durations. This is an unusual behavior, considering the typical responses of the limit-cycle oscillators associated to the majority of the biological rhythms. The dimension of an oscillator determines the PRC types that a system, submitted to pulses at different phases, can present. Simple clocks are associated to a sequence of discrete linked events, each event leading to the next and playing a functional role in generating the rhythmicity. They are unidimensional systems and can\'t present Type O PRCs and singularities, as the two-dimensional limit cycles. Based on the properties of the experimental curves and knowing the phisiological bases of these insect rhythms, we propose a simple clock model for the infradian rhythms studied here.

No description available.

acase@tulane.edu

Chronic Ang II infusion enhances proximal angiotensinogen (AGT) synthesis, secretion as well as urinary excretion. Increased luminal AGT may lead to increased intraluminal Ang II formation if renin and angiotensin converting enzyme are available. Because renin has been localized in cortical collecting duct cells, the present study was designed to determine if renin exists in medullary nephron segments of normal rat kidneys and is regulated in Ang II-dependent hypertension. Renal renin protein and mRNA expressions in sham operated and chronically Ang II-infused (80ng/kg/min, 13 days) rats were evaluated with immunohistochemistry, Western blot, RT-PCR and real time qRT-PCR techniques. Ang II infusion increased SBP (183.6 +/- 3 vs 120.8 +/- 4 mmHg) and led to marked suppression of plasma renin activity (0.9 +/- 0.3 vs 7.5 +/- 0.5 ngAngl&middot;mL&middot;h-1 ) compared to Sham-operated rats. No significant difference was observed in plasma Ang II concentration between Ang II-infused and Sham-operated rats (90.8 +/- 31.9 versus 77.6 +/- 18 fmol/mL) after 13 days of Ang II infusion. However, kidney Ang II contents were significantly higher than plasma levels in Sham-operated rats (111.8 +/- 9.3 versus 77.6 +/- 18; P < 0.05) and even further in Ang II-infused rats (221.7 +/- 15.3 versus 90.7 +/- 31.9, P < 0.01). In addition, Ang II kidney levels were significantly higher in Ang II-infused than Sham-operated rats (221.7 +/- 15.3 versus 111.8 +/- 9.3; P < 0.001). Immunohistochemical evaluation of renin showed marked suppression in juxtaglomerular (JG) cells in Ang II-infused rats compared to sham (0.14 +/- 0.05 vs 1.0 +/- 0.11DU P < 0.001). Renin was colocalized with aquaporin 2 on the apical side of principal cells. Spatial density of collecting duct segment renin immunoreactivity was higher in Ang II-infused than sham (6.40 +/- 1.4 vs 1.0 +/- 0.1 cortex; 2.5 +/- 0.3 vs 1.0 +/- 0.2DU medulla; P < 0.001) rats. Western blot analysis of kidney medulla protein showed an enhancement of renin protein expression in Ang II-infused rats in comparison to the Sham-operated rats (1.22 +/- 0.4 vs 1.0 +/- 0.1; P < 0.05). In contrast, Ang II infusion significantly decreased renin expression in kidney cortex (0.43 +/- 0.2 compared to 1.0 +/- 0.4 densitometric ratio in Sham rats; P < 0.001). Renin 1c mRNA detected in kidney medulla by RT-PCR was not inhibited by Ang II infusions as observed in kidney cortex using real time qRT-PCR (0.31 +/- .05 vs 0.28 +/- 0.04, medulla; 0.26 +/- 0.01 vs 1.00 +/- 0.31, cortex). Additional immunohistochemistry and Western blot experiments performed on isolated cortical collecting duct (M-1) cells confirmed the presence of renin. Ang II treatment (10-7M) applied on M-1 cells by the apical side showed a tendency to enhance the protein renin levels. In conclusion, this study demonstrates that Ang II infusion stimulates renin protein expression in principal cells of cortical and medullary collecting ducts. Detection of renin transcript in renal medulla which is devoid of JG apparatus indicates that renin is synthesized in this region. The enhancement in collecting duct renin provides a mechanism by which Ang I can be generated from proximally delivered AGT and thus contribute to the increased intratubular Ang II levels in Ang II-dependent hypertension / acase@tulane.edu

acase@tulane.edu

acase@tulane.edu

Experiments were performed in conscious rats to assess the contribution of V$\sb2$-vasopressinergic receptor activation to enhancement of baroreceptor reflex (BRR) sensitivity observed with vasopressin (AVP). All rats were chronically instrumented for measurement of cardiac output, arterial blood pressure and heart rate. Initial experiments were designed to determine if either blockade or activation of V$\sb2$-receptors alter BRR sensitivity. Administration of a specific V$\sb2$-receptor antagonist prior to AVP infusion diminished BRR sensitivity observed with AVP infusion. Administration of a specific V$\sb2$-receptor agonist enhanced BRR sensitivity compared to control. Further, treatment with either the V$\sb2$-antagonist or a specific V$\sb1$-antagonist prior to V$\sb2$-agonist infusion diminished the enhancement of BRR sensitivity observed with V$\sb2$-agonist administration. Finally, administration of either V$\sb2$- or V$\sb1$-antagonist prior to saline vehicle infusion did not diminish BRR sensitivity, indicating that basal levels of circulating vasopressin do not appear to affect BRR sensitivity. A second set of experiments was designed to asses the contribution of non-BRR mechanisms to the enhanced bradycardic response during V$\sb2$-agonist infusion. Although V$\sb2$-agonist infusion enhanced the bradycardic response to pressor doses of phenylephrine in intact rats, there was no effect in barodenervated rats. However, administration of pressor doses of AVP to barodenervated rats elicited a dose dependent bradycardia. A final set of experiments was designed to determine the physiological significance of vasopressinergic enhancement of BRR sensitivity. Vasopressinergic antagonists were administered during two situations of stimulated endogenous release of AVP: water deprivation and nonhypotensive hemorrhage. BRR sensitivity was not affected by water deprivation or by vasopressinergic antagonism prior to and following water deprivation. However, nonhypotensive hemorrhage enhanced BRR sensitivity, and either V$\sb2$- or V$\sb1$-antagonist administration attenuated the enhancement of BRR sensitivity. These data suggest that (1) either V$\sb2$-antagonist administration during AVP infusion or V$\sb2$-agonist administration alter BRR sensitivity, however, the specificity of the receptor activation is uncertain; (2) enhancement of bradycardic responses to pressor stimuli during V$\sb2$-agonist administration is indeed a baroreflex dependent phenomenon, although there may be a bradycardic response to AVP which is BRR-independent; and (3) BRR sensitivity may be enhanced in some situations of stimulated endogenous release of AVP, however, the specificity of the receptor activated is uncertain / acase@tulane.edu

acase@tulane.edu