1. Plasma levels of atrial natriuretic peptide and several other hormones were measured and related to the renal responses to chronic changes in the dietary intake of protein and sodium, alone and in combination. Eight healthy subjects consumed four diets for 1 week: a basal diet containing 140 mmol of sodium/day and 1 g of protein day −1 kg −1 , the same diet with isocaloric addition of 1 g of meat protein day −1 kg −1 , the basal diet with addition of 170 mmol of sodium chloride/day and the basal diet with both additions. 2. Creatinine clearance was increased significantly both by protein and, to a smaller extent, by sodium. Plasma atrial natriuretic peptide and the urinary excretion of guanosine 3′:5′-cyclic monophosphate were increased significantly by sodium but were not affected by protein. Protein induced a significant rise in plasma glucagon levels, whereas the rise in somatomedin C (insulin-like growth factor I) just failed to reach statistical significance. 3. These findings demonstrate that atrial natriuretic peptide does not mediate chronic protein-induced hyper-filtration, although it may contribute to the renal effects of sodium. Glucagon and somatomedin C (insulin-like growth factor I) may have contributed to chronic protein-induced hyperfiltration.

1. Changes in forearm blood flow to intra-arterial infusion of isoprenaline and the chronotropic response to intravenous boluses of isoprenaline were measured in 15 healthy volunteer subjects, eight younger than 25 years and seven older than 50 years. Intra-arterial blood pressure and basal plasma renin activity, adrenaline and noradrenaline were also measured. 2. Young subjects exhibited a greater increase in forearm blood flow than old subjects, to all four doses of isoprenaline used, a greater cardiac isoprenaline responsiveness (measured by the increase in heart rate; P <0.001) and a higher renin ( P <0.02). 3. Resting values of blood pressure, forearm blood flow, adrenaline and noradrenaline were not significantly different in young and old subjects. In the latter, noradrenaline correlated with forearm blood flow ( r = −0.77, P <0.05), forearm vascular resistance ( r = 0.86, P <0.02) and mean arterial pressure ( r = 0.83, P <0.02), whereas in the younger subjects forearm blood flow was related to adrenaline ( r = 0.78, P <0.05). 4. These data provide evidence for an age-related parallel reduction in cardiac, peripheral vascular and renal β-adrenoceptor-mediated responses.

1. The relationships between plasma noradrenaline concentration at rest and blood pressure, as well as increase in forearm blood flow in response to a brachial artery infusion of the α-adrenoreceptor-blocking agent phentolamine, were investigated in hypertensive and normotensive subjects of similar age. 2. In 44 hypertensive patients plasma noradrenaline correlated with systolic, diastolic and mean blood pressures, but no difference in the mean plasma noradrenaline concentration was found. 3. In 11 patients and 14 normotensive subjects α-adrenoreceptor blockade resulted in a similar increase in forearm blood flow. Only in the patients, however, was this increase related to plasma noradrenaline and blood pressure. 4. In patients with established essential hypertension plasma noradrenaline can be considered to be a marker of α-adrenoreceptor-mediated vasoconstriction, which, in part, determines the height of the blood pressure.

1. Blood pressure, systemic haemodynamics, plasma volume, renin and aldosterone were measured during placebo treatment and after 1, 4 and 12 weeks of hydrochlorothiazide in 13 patients with uncomplicated essential hypertension. Nine of these patients were also studied after 24 and 36 weeks of treatment. 2. Mean arterial pressure was lowered significantly during hydrochlorothiazide treatment. In seven patients the fall in mean arterial pressure was greater than 10% (responders); four of these were studied for 36 weeks. The remainder were considered non-responders. 3. Hydrochlorothiazide lowered cardiac output. The maximal decrease was observed after 12 weeks of treatment ( P < 0·01). In responders this was followed by a return to pretreatment values and a significant decrease in total peripheral resistance, whereas in non-responders cardiac output remained reduced and total peripheral resistance was permanently elevated. 4. Changes in plasma volume, renin and aldosterone were not significantly different in responders and non-responders although non-responders tended to show a greater degree of plasma volume depletion and a more pronounced increase in plasma aldosterone. 5. Thus it is unlikely that the initial decrease in cardiac output is an important determinant of the long-term haemodynamic effect of thiazide diuretics.

1. Renal blood flow, glomerular filtration rate, renal vascular resistance and filtration fraction were studied in ten patients with essential hypertension, during placebo, and after 1 week, 3, 6 and 9 months of hydrochlorothiazide. Plasma renin concentration and urinary excretion of vanillylmandelic acid were also measured. 2. Mean arterial pressure was lowered significantly during hydrochlorothiazide, the long-term effect being slightly more pronounced than the short-term effect. 3. The decrease in renal blood flow during the first week ( P < 0·01) was followed by a progressive rise. After 9 months renal blood flow was above placebo level in eight of the ten patients. After an initial decrease, glomerular filtration rate returned gradually to its original value. Renal vascular resistance and filtration fraction increased during the first week and declined thereafter. After 3, 6 and 9 months renal vascular resistance was significantly lower compared with placebo values. 4. Plasma renin concentration and urinary excretion of vanillylmandelic acid increased significantly during the first week of hydrochlorothiazide. Subsequently, vanillylmandelic acid fell to below pretreatment amounts ( P < 0·05), whereas plasma renin concentration remained elevated. 5. Long-term treatment of essential hypertension with hydrochlorothiazide has a favourable effect on abnormal renal haemodynamics. Besides the influence of blood pressure reduction per se , humoral and neural factors may be involved.