Biochemical changes associated with development and reversal of cardiac hypertrophy in spontaneously hypertensive rats.

This study is the first report describing the sequence of biochemical alterations of myocardium during the progression of naturally occurring hypertrophy in spontaneously hypertensive rats (SHRs) and then with its reversal by alpha-methyldopa therapy. Changes in DNA, RNA, hydroxyproline, as well as incorporation of 14C lysine into cardiac myosin, were compared with the pattern found in suitably matched controls. A significant increase in RNA, hydroxyproline, and 14C incorporation was observed in SHRs.

Use of systolic time intervals in studying hypertension.

Systolic time intervals were measured in 54 hypertensive patients divided into three groups according to severity of hypertension, variability of blood pressure levels and presence or absence of a hyperkinetic heart. The three groups were: borderline hypertension (BLH), fixed essential hypertension (FEH) and hyperkinetic essential hypertension (HEH). Systolic time intervals (STI) provided information indicating an increased cardioadrenergic drive in BLH and HEH.

Haemodynamic effects of propranolol in hypertension: a review.

Like hypertension which is a multifactorial disease, the blood pressure response to propranolol cannot be explained by one mechanism alone to the exclusion of all others. Acute (intravenous) administration of propranolol lowers cardiac output and slows heart rate but does not significantly alter blood pressure. With continued therapy however, blood pressure (in responders) is gradually reduced while cardiac output and rate remains low, indicating a readaptation of total peripheral resistance (TPR) to the new haemodynamic conditions.

Selective hypoaldosteronism despite prolonged pre- and postoperative hyperreninemia in primary aldosteronism.

In a prospective study of 7 patients with aldosterone-producing adenoma (APA), long-term (6-72 months) preoperative stimulation of plasma renin activity (PRA) by diuretic therapy (spironolactone plus hydrochlorothiazide) did not prevent selective aldosterone deficiency postoperatively. In all patients aldosterone excretion rate (AER) fell to subnormal values (from a mean of 97 to 2.6 mug/24 h) following removal of APA, although PRA remained elevated.

Dissociation between renin and arterial pressure responses to beta-adrenergic blockade in human essential hypertension.

Studies were carried out in 69 patients with essential hypertension to examine the relationship between changes in plasma renin activity (PRA) and arterial pressure (BP) in response to a beta-adrenergic blocking agent, propranolol. PRA had no consistent relationship with BP during treatment, either in patients receiving propranolol alone (r = 0.12) or in those receiving a combination of diuretics and propranolol (r = 0.

Hyperkinetic heart in severe hypertension: a separate clinical hemodynamic entity.

A long-term study of established hypertension helped identify a well defined group of 10 patients who differed both clinically and hemodynamically from 59 patients with the more frequent form of this disease. Their cardiac output was significantly increased (P less than 0.001) despite a severe elevation of arterial pressure (average 212/125 mm Hg plus or minus 13.

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

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.

Beta-adrenergic blockade in diuretic-treated patients with essential hypertension.

The influence of beta-adrenergic blockade (160 mg per day of propranolol for four weeks) on plasma renin activity, plasma volume, and arterial pressure was explored in 20 patients with essential hypertension with hyper-reninemia from long-term diuretic therapy. In 15 of these patients renin activity remained elevated (range, 3.1 to 23.