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The landmark report by de Bold et al. in 1981 signified the heart as one of the endocrine organs involved in fluid and salt balance (de Bold AJ, Borenstein HB, Veress AT, Sonnenberg H. 28: 89-94, 1981). Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) are secreted from cardiomyocytes in response to cardiac stretch as in the case of heart failure, whereas C-type natriuretic peptide (CNP) is secreted from endothelial and renal cells in response to cytokines and endothelium-dependent agonists, such as acetylcholine. Binding ANP or BNP to natriuretic peptide receptor A induces cyclic guanylyl monophosphate as second messenger in the target cells to mediate the following: natriuresis; water diuresis; increasing glomerular filtration rate; decreasing systemic sympathetic activities; plasma volume; cardiac output and blood pressure; and curbing mitoses of heart fibroblasts and hypertrophy of cardiovascular muscle cells. ANP, BNP, and CNP are cleared from the bloodstream by natriuretic peptide receptor C and degraded by an ectoenzyme called neprilysin (NEP). The plasma levels of BNP are typically>100 pg/ml in patients with congestive heart failure. Sacubitril/valsartan is an angiotensin receptor NEP inhibitor that prevents the clinical progression of surviving patients with heart failure more effectively than enalapril, an angiotensin-converting enzyme inhibitor. A thorough understanding of the renal and cardiovascular effects of natriuretic peptides is of major importance for first-year medical students to gain insight into the significance of plasma levels of BNP in patients with heart failure.

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The concentrations of tissue plasminogen activator (t-PA), urokinase plasminogen activator (u-PA) and plasminogen activator inhibitor (PAI-1) have been determined in endometrial curettings obtained from 46 subfertile women during proliferative, early or late secretory phases of the menstrual cycle. t-PA activity and antigen concentrations was significantly higher (P < 0.001) in late secretory endometrium than in proliferative or early secretory endometrium. Higher concentrations of PAI-1 antigen (P < 0.05) were also noted in late secretory phase than in proliferative and early secretory endometrium. However, u-PA concentration was not significantly different and no PAI activity could be demonstrated in the menstrual phases studied. Zymography studies confirmed the presence of both t-PA and u-PA in the endometrium. Ovarian hormonal patterns may therefore influence the activity of plasminogen activators especially of t-PA in the endometrium during various phases of the menstrual cycle.

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Die in vier Stufen erhaltenen Aminosäureester (VII) werden auf ACE‐ inhibierende Wirkung und hypotensive Effekte untersucht; die Verbindung (VIIa) ähnelt in ihrer Wirkung Enalapril.

The objective of this study was to examine the effect of sodium depletion on basal sympathetic adrenergic vascular tone and vasoconstrictor responses to adrenergic nerve stimulation and norepinephrine in pentobarbital-anesthetized dogs. Mean arterial pressure, tibial blood flow, and tibial vascular resistance were not significantly different between sodium-replete and sodium-deplete dogs. However, plasma renin activity (PRA) was 11-fold higher in sodium-deplete dogs (P less than 0.01). Sympathetic denervation in sodium-replete and -deplete dogs resulted in a similar decrease in tibial vascular resistance. Nerve stimulation at 0.25 and 0.5 Hz caused 40 +/- 5 and 48 +/- 5% decreases, respectively, in tibial blood flow in sodium-replete dogs and 71 +/- 3 and 77 +/- 3% decreases, respectively, in sodium-deplete dogs (P less than 0.01). Responses to norepinephrine administered intra-arterially were similar in both groups. Neither captopril nor saralasin reduced the potentiated responses to nerve stimulation in sodium-deplete dogs. Bilateral nephrectomy 24 h prior to the experiment reduced PRA to an undetectable level in both sodium-replete and -deplete dogs and equalized the responses to nerve stimulation and norepinephrine in both groups. Because bilateral nephrectomy, but neither captopril nor saralasin, abolished the potentiated responses in sodium depletion, a renal hormone other than renin or vascular angiotensin II may be responsible for this prejunctional adrenergic potentiation.

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