Increased plasma vasopressin in low renin essential hypertension.

Abstract

SUMMARY Baseline plasma vasopressin concentrations were measured in 48 men (all 50 years old) with decreased plasma renin concentration and untreated, sustained essential hypertension and in 29 healthy normotensive men. Mean hypertensive plasma vasopressin concentration was more than twice as high as the corresponding normotensive level (15.7 ± 2.2 [SE] vs 7.5 ± 1.0 pg/ml; p < 0.001). Plasma renin concentration in the hypertensive group was reduced compared with that in the normotensive group (0.28 ± 0.04 vs 0.46 ± 0.06 Goldblatt units X 10 4 /ml). These differences appeared despite virtually identical serum osmolality, creatinine clearance, and urinary sodium excretion in the two groups. In the first 38 hypertensive subjects, arterial plasma epinephrine concentrations were significantly increased over those of the first 28 control subjects (99 ± 12 vs 68 ± 6 pg/ml; p < 0.025). In contrast to those with low renin essential hypertension, 35 men with normal renin essential hypertension (all 40 years old) had normal plasma vasopressin levels that were not significantly different from those in a comparable normotensive control group (3.7 ± 0.8 vs 3.5 ± 0.4 pg/ml). Arterial epinephrine concentrations were not significantly different between normal renin subjects and the control group. After 6 weeks of treatment with the nonselective /3-adrenergic receptor blocker oxprenolol in 11 subjects with low renin hypertension, blood pressure was reduced and the plasma vasopressin concentration fell from 27.6 ±6.4 to 13.5 ±4.2 pg/ml (p < 0.01). After 6 weeks of treatment with the /3,-selective agent atenolol in another 11 men with low renin hypertension, plasma vasopressin level fell from 16.3 ± 3.3 to 13.1 ±3.1 pg/ml, but this reduction was not significant. In pooled groups treated with /3-adrenergic blockade, plasma vasopressin level decreased more the higher its initial concentrations (r= 0.79, p< 0.001, n = 22). These findings suggest that plasma vasopressin is increased in low renin essential hypertension and may be related to sympathetic adrenal overactivity. (Hypertension 8: 506-513, 1986) KEY WORDS • blood pressure • catecholamines • sodium • osmolality • /3-adrenergic blockade • pituitary • antidiuretic hormone A RGININE vasopressin (AVP) may increase /\ blood pressure primarily by volume reten-A. \. tion, but it is also a powerful vasoconstrictive agent, even more potent than angiotensin.1 It may also participate in cardiovascular regulation, both centrally 2 and peripherally, 3 and stimulate the gain of baroreceptor reflexes. 4 Potentiation of the vasoconstrictor effect of catecholamines has been established. with mineralocorticoid excess. 6 -9 "" Deoxycorticosterone-salt hypertension will not develop in the Brattleboro rat, which lacks AVP because of a genetic defect. Blockade by either specific antiserum or competitive antagonists of AVP substantially attenuates both the development and severity of preexisting deoxycorticosterone-salt hypertension. Most recently, observations by Hay wood et al.12 point to the sy...

Hypertension in mice with transgenic activation of the brain renin-angiotensin system is vasopressin dependent

“…Therefore, the implication of vasopressin as a primary mediator of angiotensinergic hypertension simultaneously 1) identifies vasopressin as a possible mediator of other newly recognized functions of the brain RAS (e.g., metabolic control, learning and memory, etc. ); and 2) identifies angiotensinsensitive, vasopressin-producing brain structures (e.g., the supraoptic nucleus) as major cardiovascular regulatory centers that may deserve substantially more investigation for therapeutically targeting hypertension and other disorders, especially in selected human populations with low-renin hypertension (2,3,7,15,19,39,48,49,75).…”

“…Interestingly, a population of AVP-expressing neurons project from the PVN to the hindbrain and spinal cord and appear to be involved in the regulation of sympathetic nervous activity (reviewed in Refs. 1, 10, 52), suggesting a possible AVP-mediated cross-talk between these two mechanisms.Although some studies have failed to document a substantial role for AVP in blood pressure control in heterogenous groups of human subjects (49), AVP has been implicated as a significant contributor to blood pressure control in selected populations of humans (19,48). Specifically, African Americans (3), the elderly (15), and patients with congestive heart failure (19) or chronic renal failure (2) all exhibit AVP-dependent hemodynamic changes (7).…”

“…Although some studies have failed to document a substantial role for AVP in blood pressure control in heterogenous groups of human subjects (49), AVP has been implicated as a significant contributor to blood pressure control in selected populations of humans (19,48). Specifically, African Americans (3), the elderly (15), and patients with congestive heart failure (19) or chronic renal failure (2) all exhibit AVP-dependent hemodynamic changes (7).…”

Increased nocturnal sodium excretion in obstructive sleep apnoea. Relation to nocturnal change in diastolic blood pressure

“…The influence of AVP on blood pressure is controversial. Some investigators have shown a relation between blood pressure and plasma AVP, particularly when renin levels were low [32,33], whereas others have shown that although AVP levels were elevated in patients with malignant hypertension, there was no correlation between arterial blood pressure and plasma AVP [34]. We found higher mean values of AVP in hypertensive OSA patients compared with healthy controls and the mean AVP during night-time correlated with the SBP during the night, but no correlation was found between mean AVP and the severity of OSA.…”

Serum Specific Vasopressin-Degrading Activity is Related to Blood Total Cholesterol Levels in Men but not in Women

“…AVP has long been known to play a critical role in the maintenance of free-water homeostasis, but its role as a contributor to hypertension has been controversial. This effect appears to be more important among African-American hypertensive who also have low renin profiles [23]. This effect appears to be more important among African-American hypertensive who also have low renin profiles [23].…”