Current views concerning cardiac output in the genesis of experimental hypertension.

Abstract

Humoral, neural, vascular and hemodynamic factors must all be considered in the study of hypertension. None of the unitary theories have been able to explain fully the mechanisms of experimental renal or essential arterial hypertension. Studies in many animal models and hypertensive individuals have shown that the hemodynamic component is an integral part of the mosaic of factors underlying chronic hypertension. Correlations between cardiac output, blood volume and peripheral resistance have outlined different subgroups of essential hypertensives. This has permitted the application of more effective therapeutic regimes. The problem of cardiac participation in the genesis of essential or renovascular hypertension is whether the transient increases in cardiac output observed are of sufficient magnitude and duration to initiate permanently increased peripheral resistance. Cardiac output is normally highly variable, exhibiting changes greater than those measured during the first few days of experimental hypertension. It is also well documented that increased cardiac output, resulting from electrical stimulation of the splanchnic nerves or stellate ganglion over periods of weeks up to 2 mo. results in peripheral constriction which disappears soon after the stimulation is stopped. If structural change occurs, then why does the blood pressure so quickly reverts to normal. Until more is known about the problem, there is danger in placing all hypertensives into poorly defined groups such as borderline or early hypertension and hyperkinetic circulation. Definite stages of the pathogenesis of hypertension cannot be defined without further proof.