Effect of Sustained Hypernatraemia on the Renin‐aldosterone System in the Dog

Young, David B.; McCaa, Robert E.

doi:10.1111/j.1440-1681.1981.tb00157.x

Cited by 3 publications

(1 citation statement)

References 11 publications

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“…In a study similar to the present study, the same increase in sodium concentration for 6 days had no effect on arterial pressure or plasma renin activity. 27 In an acute study, Cowley and Lohmeier 28 demonstrated that a similar degree of hypernatremia did not affect the pressor response to angiotensin II in the intact dog. Furthermore, three intensively studied experimental models that typically have elevated plasma sodium concentrations (the Brattleboro rat; the lateral, ventral, third ventricle-lesioned rat; and the deoxycorticosterone-salt hypertensive rat) do not have any cardiovascular abnormalities attributed to their hypernatremia.…”

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confidence: 97%

Analysis of the cardiovascular effects of arginine vasopressin in conscious dogs.

Tipayamontri¹,

Young²,

Nuwayhid³

et al. 1987

Hypertension

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SUMMARYThe effects of physiological elevations in arginine vasopressin on the cardiovascular system were studied in a group of nine conscious, chronically instrumented dogs. The animals were studied under normal conditions (plasma vasopressin, 4.1 ± 0.4 pg/ml), after 24 hours of dehydration (plasma vasopressin, 7.3 ±1.5 pg/ml), after a 30-minute vasopressin infusion at 2.6 ng/kg/min (plasma vasopressin, 62.8 ± 10.3 pg/ml), and after a 4-day vasopressin infusion at 2.6 ng/kg/min (plasma vasopressin, 96.6 ±8.1 pg/ml). These increases in vasopressin concentration resulted in no change in arterial pressure and significant changes in the following: a 13 and 29% decrease in resting cardiac output during dehydration and acute infusion, respectively; a 26% reduction in heart rate during acute infusion; a 12 and 54% increase in total peripheral resistance during dehydration and acute infusion; a 16 and 22% reduction in mean circulatory filling pressure during dehydration and chronic vasopressin infusion. In addition, maximum pumping ability of the heart was reduced 16 and 31 % during dehydration and acute infusion, respectively. These data suggest that elevations of vasopressin such as those occurring during dehydration or volume depletion potentially may affect cardiovascular performance by three mechanisms: 1) greatly increasing resistance to flow, 2) reducing heart rate, 3) suppressing the pumping ability of the heart. A LTHOUGH the pressor capabilities of arginine /\ vasopressin (AVP) have been recognized A. JL. since 1895, the physiological role of the hormone in cardiovascular regulation remains controversial (for reviews of this subject, see References 1 and 2). In normal, conscious animals or humans, elevations in AVP concentration into the high physiological range bring about small increases in arterial pressure, in cardiovascular regulation, the results of other recent studies raise the possibility that AVP may be important in cardiovascular control, at least in some conditions. Some of the more provocative data have come from the studies of Cowley et al. 3 and Montani et al., 3 who showed that, although changes in plasma AVP concentration within the physiological range do not produce large cardiovascular alterations in intact animals, the same increases of AVP concentration in baroreceptordenervated animals or patients with impaired cardiovascular reflexes 4 have prominent cardiovascular and hemodynamic effects. Therefore, these studies suggest that in the intact animals some aspect of baroreceptor function masks the cardiovascular effects of AVP. Additionally, administration of antagonists to the vascular receptor in several experimental models of hypertension 7 "9 and during hemorrhage 10 results in transient decreases in peripheral resistance and arterial pressure. These findings suggest that AVP is an active element of cardiovascular regulation, at least in some pathophysiological conditions.Previous analyses of the effects of AVP on the cardiovascular system have dealt mainly with the effects of the hormo...

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mentioning

confidence: 97%

Analysis of the cardiovascular effects of arginine vasopressin in conscious dogs.

Tipayamontri¹,

Young²,

Nuwayhid³

et al. 1987

Hypertension

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Inhibited Breathing and Salt-Sensitive Hypertension in Women

Anderson

Chesney

2014

Psychosocial Stress and Cardiovascular Disease in Women

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Differential regulation of adrenal corticosteroids after restriction-induced drinking in rats

Wotus

Engeland

2003

American Journal of Physiology-Regulatory, Integrative and Comp

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Wotus, Cheryl, and William C. Engeland. Differential regulation of adrenal corticosteroids after restriction-induced drinking in rats. Am J Physiol Regul Integr Comp Physiol 284: R183-R191, 2003. First published October 3, 2002 10.1152/ajpregu.00027.2002.-Water-restricted rats exhibit a rapid decrease in plasma corticosterone after drinking. The present study examined the effect of restriction-induced drinking on plasma aldosterone and plasma clearance of corticosterone. Rats were water restricted for 6-7 days and then killed before or 15 min after water administration; plasma and adrenal hormones were assayed. Plasma and adrenal corticosterone decreased after drinking without a change in plasma corticosteroid-binding globulin; plasma ACTH decreased or did not change. In contrast, plasma aldosterone did not change or increased after drinking; plasma renin activity was elevated by water restriction and increased further after drinking. In another experiment, rats were adrenalectomized, and corticosterone and aldosterone were replaced with pellets and osmotic minipumps, respectively. Rats were water restricted and killed. There was a small decrease in plasma corticosterone but no change in aldosterone after drinking in adrenalectomized animals. These data suggest that changes in plasma steroids after restriction-induced drinking result from zone-specific responses of the adrenal to known secretagogues, with minimal contribution from increased plasma clearance.corticosterone; aldosterone; corticosteroid-binding globulin; steroid clearance; dehydration THE RAT ADRENAL CORTEX is divided into two morphologically and functionally distinguishable steroidogenic zones. The inner zona fasciculata/reticularis produces corticosterone in response to its primary secretagogue, ACTH, which is released from the anterior pituitary. The outer zona glomerulosa produces the mineralocorticoid aldosterone in response to multiple factors, including ANG II, an end product of the renin-angiotensin system. Increased secretion of corticosterone and aldosterone represents a homeostatic response to stressful stimuli. In contrast to the response following stress, a marked reduction in plasma and adrenal corticosterone is observed immediately after water is presented to rats restricted to a limited amount of water each day (8,18,24,31,40). Although evidence suggests that this rapid decline in corticosterone may occur though mechanisms acting at the level of the adrenal cortex (8, 40), it is not known whether restriction-induced drinking affects aldosterone in a similar manner. Previous studies have shown increases in plasma aldosterone after deprivation-induced drinking in dogs (37) and sheep (3), whereas there were no changes in plasma aldosterone after drinking in dehydrated humans (15). However, rapid changes in corticosterone and aldosterone after drinking have not been investigated concurrently in the same animal model of dehydration. Moreover, there are inconsistencies concerning the effect of dehydration alone on aldosterone secretion ...

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Effect of Sustained Hypernatraemia on the Renin‐aldosterone System in the Dog

Cited by 3 publications

References 11 publications

Analysis of the cardiovascular effects of arginine vasopressin in conscious dogs.

Analysis of the cardiovascular effects of arginine vasopressin in conscious dogs.

Inhibited Breathing and Salt-Sensitive Hypertension in Women

Differential regulation of adrenal corticosteroids after restriction-induced drinking in rats

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