Left ventricular (LV) diastolic function was investigated in three different age groups (15, 28 and 50 weeks) of paired spontaneously hypertensive (SHR) and normotensive (WKY) rats under pentobarbital anaesthesia. A time constant of LV pressure decay, represented by T, was used as an index of LV relaxation. We assessed the relationship between haemodynamic parameters and LV structural components as quantified by microspectrophotometry (MSP), using multivariate analysis. T was significantly prolonged in the 28 and 50 week old SHR compared with their normotensive counterparts (P less than 0.05 and P less than 0.01, respectively). T was prolonged by volume loading but was not affected with afterload elevation by angiotensin infusion in all age groups of the SHR and WKY. LV wall thickness was greater in the SHR at all ages and was positively correlated with T (r = 0.42, P less than 0.05). A significant correlation was found between the increase in cardiac muscle fibre and collagen, the decrease in elastin and glycoprotein, and T on multivariate analysis (r = 0.53, P less than 0.05). We conclude that LV relaxation of SHR is disturbed from a relatively young age (28 weeks), for which we consider myocardial hypertrophy and LV structural changes found by MSP as being responsible.

1. Studies were prospectively performed on 72 hospitalized patients with essential hypertension. Blood pressure was normalized within 1 week of admission in 33 patients (group I), but did not decrease in 39 patients (group II). To determine the factors that differentiate group I from group II, cardio-renal haemodynamic and endocrinological indices were evaluated using multivariate analysis. 2. Systolic, diastolic and mean blood pressures on admission were higher in group II (P less than 0.001), whose optic fundi showed more severe changes (P less than 0.001). Although group II had greater left ventricular posterior wall thickness (P less than 0.02), left ventricular mass index (P less than 0.05) and systemic vascular resistance (P less than 0.01) on echocardiography, their cardiac index and ejection fraction were comparable with those of group I. 3. Renal blood flow (P less than 0.05) and glomerular filtration rate (P less than 0.01) were lower in group II than in group I. Renal vascular resistance was more elevated (P less than 0.01) in group II than in group I. 4. After severe sodium depletion and ambulation, group I showed a greater increase in plasma noradrenaline and adrenaline (P less than 0.05). On multivariate analysis, those with lower systolic blood pressure, better renal function and more reactive sympathetic nervous system were discriminated as group I. 5. These data suggest that group I patients have lower systolic blood pressure on admission, greater sympathetic reactivity and better renal function, all of which contribute to their spontaneous blood pressure fall after admission.

The effects of captopril in several humoral factors were studied to elucidate the role of the renin-angiotensin (RA) system in arterial and venous pressures and renal function in patients with severe chronic congestive heart failure. A single oral dose of captopril in 20 subjects reduced mean arterial blood pressure from 77 to 67 mm Hg; this decrease correlated with baseline plasma renin activity (PRA). The increase in PRA and the decrease in plasma aldosterone levels after captopril were much greater in subjects with higher PRA. Plasma norepinephrine (NE) levels decreased, while those of epinephrine did not change. Peripheral venous pressure declined from 107 to 77 mm H2O; this decrease correlated with the change in NE levels. During 7-day captopril therapy, urine volume and sodium excretion increased (1145 to 1136 ml/day and 76 to 94 mEq/day) in 11 subjects in whom renal function was followed. Renal plasma flow (RPF) rose from 237 to 364 ml/min, while glomerular filtration rate did not change; the filtration fraction decreased from 32% to 23%. Simultaneous infusion of aprotinin in six of the subjects did not affect the captopril-induced increase in RPF, despite the suppression of plasma bradykinin levels. These results suggest that captopril reduces arterial blood pressure in patients with high PRA through inhibition of the RA system and dilates veins by attenuation of sympathetic nervous activity. Increased RPF and urinary sodium excretion induced by captopril might result from inhibition of the RA system; the kallikrein-kinin system or bradykinin-mediated prostaglandins do not appear to play a major role.

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