The influence of salt intake on plasma calcitonin gene-related peptide in subjects with mild essential hypertension

Abstract

Calcitonin gene-related peptide is a pleiotropic neuropeptide with potent vasodilatory properties, which interferes with renin release and might participate in cardiovascular homeostasis. We studied the influence of salt intake on the plasma concentration of calcitonin gene-related peptide, parathyroid hormone and on the renin-aldosterone system in 15 patients with mild hypertension. Each participant was studied after 1 week of high salt intake (200 mmol/day) and after 1 week of low salt intake (50 mmol/day). The order of the two diet periods was randomized and crossover. Plasma calcitonin gene-related peptide concentration was measured by radioimmunoassay after pre-extraction by reverse chromatography. Seven patients were classified as salt-sensitive and eight as salt-resistant. In the whole group the low salt intake caused a significant decrease in arterial pressure and the expected increase in plasma renin activity and in plasma aldosterone concentration. Such changes were accompanied by a significant increase in plasma calcitonin gene-related peptide. In salt-resistant patients in the sodium-replete state calcitonin gene-related peptide levels tended to be reduced in comparison with salt-sensitive patients. Sodium depletion, however, caused a more pronounced rise in plasma calcitonin gene-related peptide in salt-resistant hypertensives, who attained levels close to those in salt-sensitive hypertensives. Interestingly, in salt-resistant hypertensives changes in plasma calcitonin gene-related peptide were closely related to plasma renin activity (r = 0.71, P = 0.003), whereas no such correlation was found in salt-sensitive patients. Parathyroid hormone was not influenced by changes in salt intake. In subjects with mild hypertension calcitonin gene-related peptide is sensitive to changes in salt intake in the physiological range. Such a response seems to be linked to the individual arterial pressure response to salt, because salt-resistant patients showed reduced calcitonin gene-related peptide levels in the sodium-replete state and a more pronounced calcitonin gene-related peptide increase, closely related to plasma renin activity, during sodium deprivation.