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[Atrial natriuretic peptide and its significance for arterial hypertension]
Insights
Atrial natriuretic peptide (ANP) levels are often elevated in hypertension due to increased blood volume or atrial stretch. While ANP infusion lowers blood pressure, stimulating its natural release may not be effective in hypertension.
Area of Science:
- Cardiovascular Physiology
- Endocrinology
- Nephrology
Context:
- Atrial natriuretic peptide (ANP) is a cardiac hormone with known natriuretic, vasodilatory, and hypotensive effects.
- Its role in the pathophysiology of hypertension is a significant area of research.
- Previous hypotheses suggested ANP deficiency in hypertension, but this has not been consistently observed.
Purpose:
- To investigate the role and levels of atrial natriuretic peptide (ANP) in various models of hypertension.
- To explore the relationship between ANP plasma levels and hypertension severity, patient characteristics, and other hormonal systems.
- To assess the therapeutic potential of ANP in hypertensive conditions.
Summary:
- ANP plasma levels are elevated in several animal models of hypertension (SHR, Dahl rats, DOCA-salt, renovascular) and in some human primary hypertension cases.
- Elevated ANP is linked to intravascular volume expansion, atrial wall stretch, age, blood pressure, and left ventricular hypertrophy, showing a negative correlation with renin.
- ANP infusion effectively reduces blood pressure and enhances natriuresis in both normotensive and hypertensive individuals, though endogenous ANP stimulation may be less effective in hypertension.
- Measurement of ANP levels cannot differentiate between primary and secondary hypertension but is elevated in primary hyperaldosteronism and renal failure.
Impact:
- Findings challenge the notion of ANP deficiency in hypertension, indicating elevated levels are common and linked to disease severity.
- Demonstrates the potent blood pressure-lowering and natriuretic effects of exogenous ANP, suggesting therapeutic potential.
- Highlights potential mechanisms for ANP resistance in hypertension, such as reduced receptor sensitivity, warranting further investigation into ANP-based therapies.
Abstract:
Atrial natriuretic peptide is a recently discovered cardiac hormone with natriuretic, vasodilatory and hypotensive activities. The role of this hormone in the pathophysiology of hypertension is of particular interest. In contrast to an earlier concept, a deficiency of the atrial peptide could not be found in animal models of hypertension or in patients. ANP plasma levels were elevated in SHR with accelerated hypertension, in salt-sensitive Dahl rats, in rats with DOCA-salt-hypertension and in animals with renovascular hypertension. Elevated ANP levels under these conditions can be explained by an expansion of the intravascular volume or by an elevated atrial wall stretch induced by the hypertension itself. In patients with primary hypertension, plasma levels of the peptide are raised in some patients and are normal in others. Plasma ANP levels correlate with age, blood pressure and signs of left ventricular hypertrophy. A negative correlation is described between ANP and renin. Measurement of plasma ANP levels does not allow a differentiation between primary and secondary forms of hypertension. Elevated ANP levels are also found in primary hyperaldosteronism and in renal failure. Stimulation of ANP secretion by physical exercise and dietary salt loading is maintained in hypertension. Infusion of 1-28-hANP leads to a reduction in systemic arterial pressure in normotensives and hypertensives. The natriuresis induced by exogenous ANP is more pronounced in hypertensives. Stimulation of endogenous ANP secretion does not prevent the rise in blood pressure possibly due to a reduction in ANP receptors in target tissues.