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No description available.

Hormonal regulation of growth and of macromolecular synthesis in a variety of tissues is now well established. This dissertation addresses the role of circulating hormones, particularly epinephrine, in the physiological regulation of myocardial mass. Following hemodynamic overload of the right ventricle, the circulating epinephrine concentration increased significantly, and blood epinephrine exhibited a significant positive correlation with myocardial mass. Further, a nonspecific β-antagonist, propranolol, blocked the usual myocardial hypertrophy that occurs in response to hemodynamic overload. These studies strongly implicate β-adrenoceptors in the regulation of myocardial mass. Theoretically, a circulating myocardial trophic hormone should result in biventricular hypertrophy. We found that a selective hemodynamic overload of the right ventricle produced significant hypertrophy of both the right and the left ventricles. A biochemical marker of β-receptor activity, ornithine decarboxylase, a key regulatory enzyme in growth, showed elevated activity in both the right and left ventricles following hemodynamic overload of the left ventricle. To further evaluate possible circulating myocardial trophic hormones, we studied hypertrophy in a donor heart transplanted into the abdomen of a recipient animal. Myocardial hypertrophy of the donor heart occurred independently of innervation and of any hemodynamic parameters. Alteration in myocardial mass paralleled the extent of β-receptor activity as assessed by the administration of exogenous β-agonists or by the modulation of β-receptor number by denervation. β-Receptor activity was assessed by the ability of isoproterenol to elevate ornithine decarboxylase activity in either the donor or the recipient heart. Finally, alterations in the levels of circulating endogenous hormones in response to pulmonary artery banding of the recipient rat heart resulted in concomitant hypertrophy of both recipient and donor hearts. These studies suggest that myocardial mass is regulated by the concentration of circulating epinephrine through its effect on myocardial β-adrenoceptors. This effect may be modified by the level of other hormones such as thyroid hormone, but does not appear to be altered to any extent by myocardial innervation or by the alteration of hemodynamic parameters except as they affect the circulating level of catecholamines.

abstract: The thrill of a live performance can enhance endorphin, serotonin, dopamine, and adrenaline levels in the body. This mixture of heightened chemical levels is a result of "performance adrenaline." This phenomenon can positively and/or negatively affect a performing singer. A singer's body is her instrument, and therefore, any bodily change can alter the singing voice. The uptake of these chemicals can especially influence a central aspect of singing: breath. "Performance adrenaline" can induce shallow or clavicular breathing, alter phonation, and affect vibrato. To optimize the positive effects and counteract the negative, diaphragmatic breathing, yoga, and beta-blockers are explored as viable management tools. When managed properly, the boost offered by "performance adrenaline" can aid the singer in performing and singing. After a review of medical and psychological studies that reveal the physiological and emotional effects of endorphins, serotonin, dopamine, and adrenaline, this paper will explore the biological changes specific to vocalists and methods to optimize these effects in performance. / Dissertation/Thesis / Doctoral Dissertation Music 2015

published_or_final_version / Medical Sciences / Master / Master of Medical Sciences

Thesis (M.D.S.) -- Dept. of Dental Health, University of Adelaide, 1981. / Typescript (photocopy).

Three major systems participate in the control of the peripheral circulation: the renin-angiotensin, the arginine vasopressin (AVP) and the sympathetic nervous systems. These studies examined the roles of the AVP and the sympathetic nervous systems in the regulation of blood pressure at both the central and the peripheral level. Anatomical studies have revealed that hypothalamic neurons containing AVP extend to the nucleus tractus solitarius (NTS) in the medulla. Since the NTS is the primary site of termination of the afferent neurons of the baroreceptor reflex arc, it suggests that AVP may be involved in central cardiovascular regulation. The effect of central AVP on mean arterial pressure (MAP) and sympathetic nerve activity, estimated from plasma catecholamine levels, was investigated. The injection of AVP into the fourth cerebroventricle and NTS of conscious, unrestrained rats increased MAP and plasma noradrenaline and adrenaline levels, suggesting that AVP may act centrally at the NTS to modulate sympathoadrenal outflow. However, the injection of a selective vascular antagonist of AVP, d(CH₂)₅Tyr(Me)AVP, into the fourth ventricle or NTS did not affect MAP or plasma catecholamine levels, either in normotensive rats, in rats subjected to hypotensive stress, or in neurogenically-stressed rats. This suggests that endogenously-released AVP may not have a tonic influence on central cardiovascular regulation. The role of AVP in the control of MAP, cardiac output (CO) and its distribution was investigated in anesthetized, surgically-stressed rats. The i.v. injection of d(CH₂)₅Tyr(Me)AVP decreased MAP and total peripheral resistance (TPR), did not alter CO, and increased the distribution of blood flow (BF) to the stomach and skin. The vascular role of AVP was found to be greater in the absence of influence from the renin-angiotensin and the sympathetic nervous systems. After blockade of the renin-angiotensin system by the infusion of saralasin the AVP antagonist increased BF to the skin and muscle, while after blockade of the α-adrenergic system with the infusion of phentolamine, the AVP antagonist markedly increased BF to the muscle. Thus, the amount of vasoconstriction produced by AVP in different vascular beds was found to depend on the endogenous vasomotor tone from the renin-angiotensin and α-adrenergic systems. Cross-circulation studies were conducted to concurrently observe the peripheral and central effects of α-agonists in two anesthetized rats, designated rat A and B, respectively. The i.v. injection of clonidine into rat A was found to increase MAP and decrease HR in rat A, and reduce MAP and HR in rat B. Since the stimulation of peripheral α-adrenoceptors in rat A by clonidine increased MAP, it suggests that the effects of peripheral post-junctional α₂-adrenoceptors predominate over those of peripheral pre-junctional α₂-adrenoceptors. In contrast, the i.v. injection of the α₁-agonist, methoxamine, in rat A increased MAP and decreased HR in rat A, and increased both MAP and HR in rat B. This suggests that central α₁-adrenoceptors may mediate responses in the opposite direction to those produced by α₂-adrenoceptors. To verify the results of the cross-circulation studies in animals free of the influence of surgery and anesthesia, and to determine whether the responses to a-agonists were mediated by changes in sympathoadrenal outflow, clonidine and a more selective α₂-agonist, B-HT 920, were injected centrally in conscious rats. The i.e.v. injection of clonidine (1 µg) significantly decreased MAP and HR and slightly decreased plasma noradrenaline and adrenaline levels; however, contrary to expectations, the i.c.v. injection of B-HT 920 (1, 10 µg) increased MAP, decreased HR and slightly increased plasma noradrenaline and adrenaline levels. To determine whether the responses to central injection of clonidine or B-HT 920 were due to the stimulation of α₂-adrenoceptors, i.c.v. injections of these drugs were given after pretreatment with rauwolseine, a selective α₂-antagonist. The i.c.v. injection of rauwolscine in conscious rats increased MAP and plasma noradrenaline and adrenaline levels, suggesting that central α₂-adrenoceptors may mediate tonic inhibition of the cardiovascular system. However, i.c.v. injections of clonidine or B-HT 920 produced the same responses in the absence or presence of rauwolscine. Further studies with different α-adrenergic agonists and antagonists with various selectivities are necessary before we can explain the differential effects of central clonidine and B-HT 920. / Medicine, Faculty of / Anesthesiology, Pharmacology and Therapeutics, Department of / Graduate

published_or_final_version / Physiology / Doctoral / Doctor of Philosophy

published_or_final_version / Pharmacology / Master / Master of Philosophy