The use of cardiac peptide measurements as possible diagnostic tools in congestive heart failure has been extensively discussed in the recent literature. Therefore, the aim of this study was to establish a model of experimental chronic heart failure, and thereby perform a comparative study of secretion and circulating levels of the cardiac peptides atrial natriuretic peptide (ANP), N-terminal proatrial natriuretic peptide (N-terminal proANP) and brain natriuretic peptide (BNP) during evolving heart failure. Chronic heart failure was induced in seven pigs by rapid left atrial pacing for three weeks. The effects of failure induction were documented 24 h after pacemaker deactivation. Hemodynamic indices of cardiac preload, like pulmonary capillary wedge pressure (PCWP) and right atrial pressure (RAP), were all considerably increased compared to sham operated controls. Likewise, plasma endothelin-L, noradrenaline, renin activity, aldosterone and angiotensin II were all markedly increased. Heart failure was accompanied by significant increases in both estimated cardiac secretory rate and plasma concentrations of all three cardiac peptides, significantly correlated to the PCWP. The directional changes during evolving heart failure were similar, although the percentage increase in plasma BNP was much larger than for ANP and N-terminal proANP. In absolute molar terms, however, the BNP concentration changes were minor compared to those of the other two peptides. The larger percentage increase of BNP might indicate its superiority as a marker of heart failure development, provided a functional assay suitable for clinical use can be designed for a peptide circulating in this low concentration range.

Vasoactive humoral factors were measured in 27 patients before and during the first week of conventional treatment of acute heart failure. On admission, all patients were given frusemide intravenously, followed by oral digoxin and diuretic therapy. Before drug treatment, plasma renin activity and plasma angiotensin II concentrations were within normal ranges in the group of patients without previous diuretic treatment, but were significantly higher in those 16 patients already on diuretic drugs when admitted to hospital. After diuretic treatment, however, even the former group revealed activation of the renin-angiotensin system. Plasma concentrations of catecholamines were increased initially but normalized within 1 day. A majority of the patients initially had very high plasma concentrations of atrial natriuretic peptide (mean 276.9 +/- 39.0 pg ml-1) which decreased but did not normalize during the study period. High plasma levels of arginine vasopressin (mean 56.8 +/- 14.6 pg ml-1) were found, but tended to be reduced during treatment. Thus, patients with acute heart failure displayed increased plasma concentrations of atrial natriuretic peptide, arginine vasopressin and catecholamines, but these vasoactive hormones decreased in parallel to clinical improvement during diuretic therapy. In contrast, the renin-angiotensin system became clearly activated.

SUMMARYA study was made of water and salt balance during a 28 h period of starvation in lactating and anoestral goats. Food deprivation caused diminished water intake in all but one animal, and the secretion of urine and milk gradually decreased. The plasma volume and the glomerular filtration rate were reduced, the plasma Na concentration lowered, and the plasma renin activity and plasma aldosterone concentration raised during starvation, After 28 h without food the goats were given a load of water or saline into the rumen. The fall in the plasma protein concentration that occurred indicates that the plasma volume increased in all animals within 4 h of receiving saline, but was unchanged after the water load. The plasma Na concentration decreased further after the water load, but increased in all animals after the saline load. The plasma renin activity and plasma aldosterone concentration remained elevated after the intraruminal water load, but fell towards basic values after the saline load. The renal Na excretion decreased during food deprivation, and showed no increase within 4 h of saline loading. It appears that only the load of saline restored the salt and water homoeostasis of the animal. Lactating and anoestral goats do not apparently differ in their response to starvation. The effects of starvation on fluid balance seem to become as severe in goats as in monogastric species despite food reservoirs in the reticulo-rumen and omasum at the onset of food deprivation.

Thirteen patients with mild essential hypertension, mean age 44 years (range 21–59), were studied during “stress” before and after postsynaptic α‐adrenoceptor blockade and combined postsynaptic α‐ and non‐selective β‐adrenoceptor blockade. Loud broad band noise (100 dBA for 10 min) was used as the stress stimulus. Exposure to noise caused a significant increase in systolic (7%, p<0.05), diastolic (9%, p<0.01) and mean arterial pressure (6%, p<0.01). The blood pressure elevation was caused by an increase in total peripheral resistance (12%, p<0.05). There was no significant change in heart rate, stroke volume or cardiac output. The blood pressure response during noise stimulation was not affected by postsynaptic α‐adrenoceptor blockade (prazosin, 2 mg orally). The hemodynamic reaction pattern, however, was totally reversed. Thus, the cardiac output increased significantly (9%, p<0.05), while the total peripheral resistance tended to decrease. Combined postsynaptic α‐ and non‐selective β‐adrenoceptor blockade (la‐be talol, 200 mg orally) inhibited the increase in systolic blood pressure caused by noise, while the diastolic and mean arterial pressures still increased significantly (5%, p<0.01). Labetalol effectively blocked the stress‐induced increase in total peripheral resistance and there was no significant increase in cardiac output after combined α‐ and β‐adrenoceptor blockade. Exposure to noise caused a significant increase in circulating noradrenaline (20%, p<0.05). Plasma adrenaline and plasma renin activity were not affected by noise stimulation. These results suggest that blood pressure elevation is essential during “stress” but that the hemodynamic pattern causing blood pressure elevation may vary and may be affected by pharmacological blockade of various parts of the sympathetic nervous system.