Hormonal profile and role of nitric oxide in salt-sensitive and salt-resistant essential hypertension

Recent studies have shown that cardiovascular events and end-organ damage o ccur more frequently in patients with salt-sensitive essential hypertension (SH) than in salt-resistant essential hypertension (RH). Nitric oxide (NO) plays an important role in regulating the pressure-natriuresis relationshi p. Therefore impaired NO synthesis may produce or aggravate salt-sensitive hypertension. This study was conducted to determine the hormonal levels and nitric oxide metabolites in hypertensive patients. 25 patients underwent s alt sensitivity testing. 24 h ambulatory blood pressure was recorded after a 5-day period on low salt diet (20 mEq/d) and after a 5-day period on a hi gh salt diet (200 mEq/d). Subjects showing greater than or equal to 10 mmHg increase in mean BP when changing from low to high dietary salt intake wer e classified as salt sensitive and as salt resistant when the BP changes we re < 10 mmHg. Based on BP recordings 13 patients were characterised as whit e coat hypertension (WC), 13 patients as salt resistant (SR) and 12 as salt sensitive (SS). A significative relationship was seen between plasma gluco se-insulin concentration and body mass index. The ventricular mass index wa s similar in SS and SR patients. The plasma uric acid, triglicerides and PA I-I were elevated in SS compared with SR, and control group (C). During low sodium intake, plasma renin and aldosterone were decreased in SS compared with SR, and C. No differences in plasma catecholamines or their changes wi th intake sodium modifications were seen among the patients. During high so dium intake urinary NO excretion increased in SR (38 +/- 9 vs 18 +/- 2 mg/g creat), and C (24 +/- 2 vs 16 +/- 3 mg/g creat) (p < 0.01) but not in SS p atients (21 +/- 3 vs 26 +/- 4 mg/g creat). The NO excretion changes showed negative correlation with BP changes (r = 0.49, p < 0.01). During low sodiu m intake, SR and SS patients showed a normal nocturnal decrease of BP (dipp ers). During high sodium intake SS patients became non-dippers. Our results showed that patients with salt sensitive hypertension displayed a supresse d renin-aldosterone system, an attenuated nocturnal decline in blood pressu re on high-salt diet and an impairment of endothelial function. The relatio nship between urinary nitrate excretion and arterial pressure suggest that the salt sensitivity of arterial pressure may be related be blunted generat ion of endogenous nitric oxide.