Impaired control of vasopressin release in hypertensive subjects with cardiac hypertrophy.

Abstract

SUMMARY The effects of graded lower body negative pressure (-10 and -40 mm Hg) on vascular resistance and plasma vasopressin, norepinephrine, and renin activity were assessed in seven hypertensive subjects with left ventricular hypertrophy and seven sex-matched and age-matched normotensive subjects. In both groups increasing levels of lower body negative pressure induced a progressive decrease in right atrial pressure and an increase in vascular resistance. In normal subjects plasma vasopressin, norepinephrine, and renin activity were progressively raised, whereas only the higher level of stimulation increased plasma renin activity, norepinephrine, and vasopressin in hypertensive subjects. Propranolol induced a significant increase in plasma vasopressin in normal subjects (from 1.3 ± 0.1 to 2.0 ± 0.1 pg/ml; p<0.05) but not in hypertensive subjects. In this latter condition -10 mm Hg lower body negative pressure failed to increase plasma vasopressin, norepinephrine, and renin activity in normal subjects. Propranolol abolished the change in plasma renin activity in both groups, reduced the increase in vascular resistance induced by -40 mm Hg lower body negative pressure in normotensive subjects, but did not modify the rise in vasopressin elicited by this stimulus in normal subjects or the humoral and hemodynamic reflex responses evoked in hypertensive subjects. These results suggest that cardiopulmonary receptors are involved in the control of vasopressin release in normal subjects, whereas in hypertensive subjects with left ventricular hypertrophy, this control is altered because of an impaired function of cardiopulmonary receptors. (Hypertension 10: 595-602, 1987) KEY WORDS • propranolol • lower body negative pressure • norepinephrine A LTHOUGH the sensitivity of the nonosmotic / \ control of arginine vasopressin (AVP) release A. JL. in humans seems to be somewhat controversial, 1 " 4 recent reports 5 ' 6 support the hypothesis that factors other than blood osmolarity are involved in the regulation of AVP release in humans. In particular, Leimbach et al. 5 demonstrated that combined unloading of cardiac and arterial baroreceptors induced by lower body negative pressure (LBNP) increases plasma AVP in subjects with high plasma osmolality. Egan et al. 6 reported that the selective unloading of cardiopulmonary receptors, by thigh-cuff inflation, increases plasma AVP levels in humans. These observations raise the possibility that AVP release may be altered in patients with impaired cardiopulmonary or arterial baroreceptor reflex responsiveness.From the Istituto di Clinica Medica I, II Facolta di Medicina e Chirurgia, Universita di Napoli, Italy.Address for reprints: Bruno Trimarco, M.D., Istituto di Clinica Medica I, II Facolta di Medicina, via S. Pansini 5, 80131 Napoli, Italy.Received November 4, 1986; accepted June 30, 1987. In patients with established hypertension, we observed that the postural change from the supine to the upright position did not induce the rise in AVP plasma levels observed in normote...

Comparison between men and women of volume regulating hormones and aquaporin-2 excretion following graded central hypovolemia

“…Regarding the minimum LBNP level required to stimulate an AVP response current evidence is somewhat conflicting. Trimarco reported a very slight AVP increase in subjects which underwent -10 mmHg of LBNP for 20 minutes , a lower stimulus than our protocol using increasing levels of LBNP starting with -10 and ending with -40 mmHg (Trimarco et al 1987) . Goldsmith et al in 1982 used an experimental protocol similar to ours, monitoring central venous pressure (CVP) instead of LBNP strength and reducing a baseline CVP of 7,2 mmHg to 3.8 mmHg for 10 minutes and then to 1.0 mmHg for another 10 minutes.…”

Peroxisome Proliferator-Activated Receptor-α and Receptor-γ Activators Prevent Cardiac Fibrosis in Mineralocorticoid-Dependent Hypertension

“…22 As discussed below, the DOCA-salt rat is a model of severe hypertension associated with activation of other mechanisms, such as the sympathetic system and vasopressin, which may be involved in the development of cardiac hypertrophy. 31 As well, side effects such as fluid retention have been reported with glitazones 32 and could explain the worsening of cardiac hypertrophy induced by rosiglitazone.…”

“…33 Vasopressin plays a role in the development of hypertension 34 in our model and has been described as a hypertrophic agent on cardiac myocytes. 31,35 Recent data indicate that short-term treatment with fenofibrate prevents cardiac fibrosis and ET-1 production in a model of aortic banding in rats. 36 Moreover, PPAR-␥ activators (troglitazone and pioglitazone) partially prevented cardiac hypertrophy and ET-1 overexpres- sion in the same model.…”

Association of arginine vasopressin with low atrial natriuretic peptide levels, left ventricular remodelling, and outcomes in adults with and without heart failure

“…Despite the importance of AVP and its role in hyponatraemia in advanced HF, little is known about the non‐osmotic triggers for its release in humans with and without HF. A role for baroreceptor desensitization has been proposed as a cause for dysregulated AVP release . However, human studies assessing the association between the ANP axis and AVP levels are scarce.…”

“…A role for baroreceptor desensitization has been proposed as a cause for dysregulated AVP release. 23 However, human studies assessing the association between the ANP axis and AVP levels are scarce. Atrial natriuretic peptide, a member of the natriuretic peptide family, is released in response to atrial stretch and exerts a variety of biological effects such as natriuresis, vasodilation, and inhibition of renin-angiotensinaldosterone pathway.…”