Hemodynamic and humoral characteristics of hypertension induced by prolonged stellate ganglion stimulation in conscious dogs.

Abstract

Recent evidence has suggested that cardiac factors may play a role in the evolution of arterial hypertension. To test the possibility that an increase in cardiac-performance can lead to a sustained increase in systemic blood pressure, we electrically stimulated the left stellate ganglion of six conscious dogs continuously for a 7-day period and monitored cardiac output and arterial blood pressure. In all six dogs, stimulation elicited an abrupt rise in systemic blood pre-sure that was entirely due to rise in cardiac output that lasted at least 6 hours. After 1 day of continuous stimulation, cardiac output retured to control values, but blood pressure remained elevated. After 7 days of stimulation, blood pressure was increased by an average of 25 mm Hg and peripheral resistance by 35 plus and minus 4%. Measurements of blood volume, plasma renin activity, circulating catecholamines (three of the six dogs), and sodium balance showed that none of these factors could explain the development pf this sustained hypertension. Pharmacologic blockade with phenoxybenzamine prevented in large part the rise in blood pressure in short-term stellate ganglion stimulations, whereas propranolol had very little effect on the pressor response, although it nearly abolished the increase in cardiac output. The data indicate that continuous stimulation of the stellate ganglion in conscious dogs leads to substained rises in both blood pressure and peripheral resistance; these changes are apparently mediated by increased activity of the sympathetic nervous system.

Cardiogenic hypertension in maturing dogs.

“…This conclusion is in agreement with the observation of increased CO resulting from electrical stimulation of the stellate ganglion for periods of 1 week up to 2 months, with peripheral constriction disappearing soon after the stimulation is stopped. 1 Furthermore, the structural changes in vascular architecture, with changes in wall thickness and length and growth or retardation of new and existing vessels, postulated to underlie long-term autoregulation did not occur in the present study.…”

Neurogenic pressor episodes fail to cause hypertension, but do induce cardiac hypertrophy.

“…Previous models to cause labile hypertension had numerous shortcomings. Such invasive procedures as stimulation of the defense area 13 or the stellate ganglion 28 can be extended only over relatively short periods of time. Removal of arterial baroreceptors 16 or central destruction of the nuclei of the solitary tractus 29 tend to cause labile blood pressure where periods of hypertension are offset by periods of hypotension, and the average blood pressure is only minimally elevated.…”

Production of sustained hypertension by lesions in the nucleus tractus solitarii of the American foxhound.

“…1 production of sustained hypertension by continuous stimulation of renal and splanchnic nerves or stellate ganglia, ' 1 ' or by chronic intrarenal norepinephrine infusion 4 in conscious dogs; correlation of diastolic blood pressure with plasma concentration of norepinephrine and dopamine betahydroxylase activity in patients with essential hypertension; 6 and the common hemodynamic characteristics of patients with labile hyperterision, including tachycardia, high cardiac output, venoconstriction and normal peripheral vascular resistance. 6 "' These changes are likely to be mediated by increased activity of the sympathetic nervous system.…”