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The relation of renin-angiotensin status to general hemodynamics and to neurogenic vascular resistance was studied in patients with border-line hypertension. Plasma renin activity during standing was referred to a standard renin-urinary sodium nomogram derived from 18 normal subjects. Among 22 patients with borderline hypertension the renin level was high in 8, low in 4 and within normal limits in the remaining 10. In patients with borderline hypertension and high or normal levels of plasma renin activity, the blood pressure elevation was due to increased total peripheral vascular resistance. In contrast, in patients with low renin borderline hypertension, total peripheral resistance was not significantly elevated; the blood pressure elevation reflected a cardiac index 12 percent higher than that in normal subjects. The neurogenic contribution to total peripheral vascular resistance was assessed by studying the effects of alpha adrenergic blockade with phentolamine, after prior autonomic blockade of the heart with atropine (0.04 mg/kg body weight) and propranolol (0.2 mg/kg). Phentolamine (15 mg) produced an immediate reduction in total peripheral resistance of 12.0 +/- 6.7 percent in patients with high renin borderline hypertension (P less than 0.01) but no change in normal subjects or those with borderline hypertension and normal or low renin levels. Normalization of the blood pressure followed "total" autonomic blockade with atropine, propranolol or phentolamine only in patients with high renin borderline hypertension. It is concluded from these preliminary data that in high renin borderline hypertension the blood pressure elevation is sustained by neurogenic mechanisms. The elevated renin level in these patients is probably an expression of increased sympathetic nervous activity. Although the elevated plasma renin level may possibly be contributing to the generation of higher sympathetic tone, or data do not support a direct role of circulating angiotensin in the maintenance of the elevated vascular resistance.
A 52-year-old man was admitted to the Brigham and Women's Hospital (BWH) on August 21, 1984, for evaluation of a possible pheochromocytoma. He was first told of his hypertension at age 43 and was treated with /3-blockers, most recently nadolol (40 mg p.o q.d.) with "good control." On August 12, 1984, he was awakened from sleep with spasmotic midepigastnc pain, strong pulsations in his head, a feeling of generalized warmth, nausea, and diaphoresis. He induced vomiting, which did not improve his symptoms, and had an episode of watery diarrhea. He then went to a local hospital, where a blood pressure (BP) of 152/130 mm Hg was noted. He was treated for abdominal pain with 15 mg of morphine sulfate and 10 mg of prochlorperazine maleate (Compazine). Nadolol (40 mg daily) was continued. Results of an upper gastrointestinal series and a sulfobromophthalein function test were normal, and an abdominal ultrasono- He was transferred to BWH on August 21, 1984 He denied any history of palpitations, chest discomfort, or weight loss. On further questioning, the patient stated that he had had a premonition before each episode occurred. Past medical history included the passage of a kidney stone in 1981. Family history included a father and four siblings with onset of high BP in their midthirties. The patient was experiencing stress because of an ongoing divorce and his work as an executive in a computer company. He smoked no cigarettes, drank alcohol socially, and used no other medications On admission, the following BP measurements were recorded: supine, right arm, 190/110 mm Hg, left arm, 170/110 mm Hg, pulse, 60 beats/min; standing, 96/50 mm Hg, pulse, 100 beats/min. Fundi showed artenolar narrowing; lungs were normal. The carotid arteries were without bruits, and examination of the heart revealed no murmur or gallop. Results of an abdominal examination were normal. The ECG was normal. Results of laboratory studies (Tables 1 and 2) were normal except for serum glutamic-oxaloacetic transaminase levels of 128 U/L, serum glutamic-pyruvic transaminase levels of 216 U/L, and alkaline phosphatase levels of 148 U/L. While at the BWH, the patient had no further episodes.
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