Plasma Vasopressin Variation and Renin Activity in Normal Active Humans

Katz, Fred H.; Smith, Justin A.; Lock, John Paul; Loeffel, D.E.

doi:10.1159/000179011

Cited by 28 publications

(9 citation statements)

References 18 publications

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“…Neuronostatin-induced sympathoactivation also likely affects the release of AVP from the posterior pituitary, since an increase in arterial pressure can inhibit AVP secretion (17). The latter explanation is more plausible, since vasopressin can be rapidly released in response to orthostatic changes (12). However, in our experiments, an initial increase, not a decrease as in hypotensive events, was observed, and thus, the baroreflex activation of AVP secretion would not have occurred.…”

Section: Discussionmentioning

confidence: 54%

Neuronostatin acts in brain to biphasically increase mean arterial pressure through sympatho-activation followed by vasopressin secretion: the role of melanocortin receptors

Yosten

Pate

Samson

2011

American Journal of Physiology-Regulatory, Integrative and Comp

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Neuronostatin is a recently described neuropeptide that is derived from the somatostatin preprohormone. We have shown previously that neuronostatin led to a biphasic, dose-related increase in mean arterial pressure when injected into the lateral cerebroventricle of adult, male rats. Because neuronostatin depolarized both magnocellular and parvocellular, paraventricular nucleus neurons in hypothalamic slice preparations, we hypothesized that neuronostatin elevated mean arterial pressure first by stimulating sympathetic nervous system activity followed by the release of a pressor hormone, specifically vasopressin. We found that the first phase of neuronostatin-induced increase in mean arterial pressure was reversed by pretreatment with phentolamine, indicating that phase 1 was, indeed, due to an increase in sympathetic activity. We also found that centrally injected neuronostatin led to a dose-related increase in vasopressin secretion in a time course consistent with the peak of the second phase. Furthermore, the second phase of arterial pressure elevation was reversed by pretreatment with a vasopressin 1 receptor antagonist, indicating that phase 2 was likely due to an increase in vasopressin secretion. We previously have shown that the anorexigenic and antidipsogenic effects of neuronostatin were reversed by pretreatment with the melanocortin 3/4 receptor antagonist, SHU9119, so we evaluated the ability of SHU9119 to reverse the effects of neuronostatin on MAP and vasopressin secretion. We found that SHU9119 abrogated the second phase of neuronostatin-induced increase in MAP and neuronostatin-induced vasopressin secretion, indicating that neuronostatin acts through the central melanocortin system to increase vasopressin release, ultimately leading to an elevation in MAP.

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Section: Discussionmentioning

confidence: 54%

Neuronostatin acts in brain to biphasically increase mean arterial pressure through sympatho-activation followed by vasopressin secretion: the role of melanocortin receptors

Yosten

Pate

Samson

2011

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Indeed, a strong correlation exists between diurnal variations in this cardiovascular parameter and plasma norepinephrine and epinephrine levels, suggesting that the sympathetic system drives blood pressure circadian rhythms (105,123,136). It should also be noted that additional cardiovascular reactive peptides (e.g., atrial natriuretic peptide, vasopressin, and components of the renin-angiotensin system) exhibit considerable diurnal variations and therefore potentially influence blood pressure circadian rhythms (43,62,63,100). Whether the circadian clock within the cells of the cardiovascular system influences responsiveness to these neurohumoral factors, thereby contributing to circadian rhythmicity in blood pressure, is an attractive possibility that awaits investigation.…”

Section: Environmental Versus Intrinsic Influences On Cardiovascular mentioning

confidence: 99%

The circadian clock within the heart: potential influence on myocardial gene expression, metabolism, and function

Young

2006

American Journal of Physiology-Heart and Circulatory Physiology

182

136

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It is becoming increasingly clear that the intrinsic properties of both the heart and vasculature exhibit dramatic oscillations over the course of the day. Diurnal variations in the responsiveness of the cardiovascular system to environmental stimuli are mediated by a complex interplay between extracellular (i.e., neurohumoral factors) and intracellular (i.e., circadian clock) influences. The intracellular circadian clock is composed of a series of transcriptional modulators that together allow the cell to perceive the time of day, thereby enabling preparation for an anticipated stimulus. These molecular timepieces have been characterized recently within both vascular smooth muscle cells and cardiomyocytes, giving rise to a multitude of hypotheses relating to the potential role(s) of the circadian clock as a modulator of physiological and pathophysiological cardiovascular events. For example, evidence strongly supports the hypothesis that the circadian clock within the heart modulates myocardial metabolism, which in turn facilitates anticipation of diurnal variations in workload, substrate availability, and/or the energy supply-to-demand ratio. The purpose of this review is therefore to summarize our current understanding of the molecular events governing diurnal variations in the intrinsic properties of the heart, with special emphasis on the intramyocardial circadian clock. Whether impairment of this molecular mechanism contributes toward cardiovascular disease associated with hypertension, diabetes mellitus, shift work, sleep apnea, and/or obesity will be discussed.

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“…This antiserum has virtually no cross-reactivity with oxytocin and vasotocin. Its specificity has been detailed elsewhere (16,17). Sensitivity of the assay using this antiserum in our laboratory was usually 0.1 and always 0.2 pg/assay tube, and the 50% displacement was 5 pg/assay tube.…”

Section: Osmolalitymentioning

confidence: 99%

“…The mean body weight of rats during gestational day [17][18][19][20] (average 10±3 pups per litter) was 283±27 g (n = 17) compared with 209±29 g (n = 19) in age-matched virgin controls (P < 0.001).…”

Section: Brattleboro Rats With Hereditary Diabetes Insipidusmentioning

confidence: 99%

Osmoregulation during Pregnancy in the Rat

Dürr¹,

Stamoutsos²,

Lindheimer³

1981

J. Clin. Invest.

125

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AB S T R A C T Osmoregulation was studied in near term and age-matched Sprague-Dawley rats. Basal plasma osmolality (Posm) and plasma sodium (PNa) were 281+3 mosmol/kg and 134+3 meq/liter, respectively, on the 20th gestational day compared with 292+±3 mosmol/kg and 140+1 meq/liter in virgin animals (P < 0.001), whereas Purea and plasma water content were similar in pregnant and control rats. These differences could not be reproduced in animals receiving progesterone, estrone, or a combination of progesterone and estradiol for 2 wk.Pregnant and control rats were deprived of water for changes (A%) were significantly greater in the gravid animals (P < 0.01). Therefore, Posm was increased without concomitant volume depletion by intraperitoneal hypertonic saline. Again PAVP VS. Posm correlated significantly (r > 0.9; P < 0.001) in each group, and the apparent threshold was 14 mosmol lower in pregnant animals. Diluting ability, tested by oral water loading, was not impaired in the pregnant animals which excreted a 30 ml/kg load as well as controls. Also, chronically hydrated virgin animals whose fluid intake was more than twice that of pregnant rats (for 19 d) did not lower their Posm.In separate studies homozygous Brattleboro rats, which produce no endogenous vasopressin, were also shown to have a decreased Posm (pregnant 292 +4 mosmol/kg; virgin 310+6 mosmol/kg P < 0.001), but unchanged Uosm during pregnancy.Data demonstrate a resetting ofthe osmostat in gravid Sprague-Dawley rats as Posm and the threshold for AVP secretion both decrease significantly during gestation in this species. Studies in homozygous Brattleboro animals with hereditary diabetes insipidus suggest that the osmotic threshold for thirst is reset as well. INTRODUCTION Plasma osmolality decreases during normal human pregnancy to values that range 5-10 mosmol/kg below that of nonpregnant women (1-3). This decrement is apparent by the 6th gestational wk and is sustained until term. If such a reduction in osmolality occurred in a nongravid subject she would cease secreting antidiuretic hormone (ADH)l and enter a state of con-

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Plasma Vasopressin Variation and Renin Activity in Normal Active Humans

Cited by 28 publications

References 18 publications

Neuronostatin acts in brain to biphasically increase mean arterial pressure through sympatho-activation followed by vasopressin secretion: the role of melanocortin receptors

Neuronostatin acts in brain to biphasically increase mean arterial pressure through sympatho-activation followed by vasopressin secretion: the role of melanocortin receptors

The circadian clock within the heart: potential influence on myocardial gene expression, metabolism, and function

Osmoregulation during Pregnancy in the Rat

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