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This study was designed to investigate the possibility of sex and age differences in the insulin-blood pressure relationship in a general Japanese population with a wide age range. Fasting serum insulin, lipids, plasma glucose, blood pressure and anthropometric measurements were made on 1,537 men and 843 women aged 16 to 65 years. Of the 2,380 subjects in the present analysis, 290 (184 men, 106 women) were hypertensive. When divided into four age groups (16 to 17, 21 to 22, 30 to 49 and 50 to 65 years), the male hypertensive subjects were found to have significantly higher fasting insulin levels, triglycerides levels and body mass index and lower glucose/insulin ratios than normotensive male subjects in all age groups. In the women, there was no significant difference in serum insulin levels or glucose insulin ratios between the hypertensive and normotensive groups in any age group. Simple correlation analysis showed that blood pressure was statistically significantly correlated with serum insulin levels and body mass index in the men in all age groups. In women, the correlation between blood pressure and serum insulin was insignificant in the 21- to 22-year-old age group. In men but not women, multivariate analysis showed that blood pressure was significantly and independently correlated with fasting serum insulin levels. The results of this study suggests the existence of sex and age differences in the insulin-blood pressure relationship in a Japanese population.

The evidence that some older patients with essential hypertension have low urinary dopamine excretion has brought into question the levels of urinary dopamine and plasma dopa, the major source of urinary dopamine, in young patients with essential hypertension. Twenty-four-hour urine sodium, creatinine, dopamine and noradrenaline and plasma dopa were evaluated in 48 patients with essential hypertension aged 18 to 27 years and 25 normotensive subjects. In comparison with age-matched normotensive subjects, the hypertensive patients had higher urinary dopamine (1920 +/- 80 vs 1520 +/- 130 nmol/day, p < 0.01) and noradrenaline (216 +/- 11 vs 179 +/- 12 nmol/day, p < 0.05) excretion. There was a significant correlation between urinary dopamine and noradrenaline excretion. There was no difference in plasma dopa levels between normotensive and hypertensive subjects. These results suggest that the elevated conversion of dopa to dopamine in the kidney is leading to increased urinary dopamine excretion in young patients with essential hypertension.

The effects of L-dopa on blood pressure, heart rate, plasma renin activity, norepinephrine, epinephrine and prolactin were studied in a randomized single-blind trial in 36 patients with essential hypertension. In response to L-dopa, 250 mg administered orally, the blood pressure decreased significantly as compared with the results of placebo treatment. The heart rate and plasma norepinephrine and epinephrine were unchanged. The plasma renin activity and prolactin decreased as a result of L-dopa administration. The administration of a peripheral DA2 dopamine receptor blocker, domperidone (20 mg, orally) prevented the L-dopa-induced reduction in plasma prolactin but failed to block the fall in blood pressure and plasma renin activity. These results suggest that the blood pressure-lowering effect of L-dopa may be mediated through multiple sites involving D1 dopamine receptors, the central nervous system, and the renin-angiotensin system.

The effects of the angiotensin-converting enzyme inhibitor captopril on blood pressure, heart rate, plasma prolactin, and renin activity were examined in a single-blind, placebo-controlled trial on 30 patients with essential hypertension (15 given drug, 15 placebo). Captopril, 25 mg administered orally, reduced the blood pressure and increased the plasma renin activity. Captopril decreased mean plasma prolactin from 17.5 +/- 1.4 ng/mL to 9.1 +/- 1.0 ng/mL (p less than 0.001). Significant correlation was found between captopril-induced change from control values of plasma prolactin (delta plasma prolactin) vs delta plasma renin activity (r = -0.688, p less than 0.001). These results suggest that acute administration of captopril was accompanied by a reduction in plasma prolactin and that this reduction may be of clinical significance during therapy of hypertension.

Plasma and urine norepinephrine, epinephrine and home blood pressure were measured in 48 young hypertensive men (mean age, 21 years) and 25 matched normotensive controls. Plasma samples were drawn following 30 min rest in the clinic and 24 h urine samples were collected at home. Twenty-one hypertensive patients were given a single dose of clonidine (150 micrograms orally). Changes in blood pressure, heart rate and plasma norepinephrine were assessed. Twenty-five of the hypertensive patients were found to have a normal home blood pressure (defined from records of the normotensive subjects). The other group of patients maintained a high home blood pressure. In comparison to normal subjects, patients with a high home blood pressure were characterized by higher urinary norepinephrine and epinephrine excretion and higher plasma epinephrine. Patients with a normal home blood pressure had normal heart rate at home, normal plasma and urinary catecholamines. However, the two groups of hypertensives could not be distinguished on the basis of clinic blood pressure, plasma or urinary catecholamines due to considerable overlap. At 90 min after oral clonidine administration, the plasma norepinephrine and blood pressure levels were decreased in both groups of hypertensives to a similar extent. The changes in heart rate were significantly smaller in patients with a high home blood pressure than in those with a normal home blood pressure. These results suggest that the patients with a high home blood pressure tended to have a high sympathetic nerve activity. However, the two groups of hypertensives could not be separated on the basis of plasma or urinary catecholamine measurements.

The possibility that a familial background of hypertension might influence the blood pressure response to a calcium entry blocker was evaluated in 15 normotensive relatives of patients with essential hypertension and 18 normotensive subjects with no family history of hypertension. Under control conditions, blood pressure, heart rate, plasma noradrenaline, adrenaline, and renin activity did not differ between the two groups. Nifedipine, at a dose of 10 mg administered sublingually, lowered the blood pressure and increased the heart rate, plasma noradrenaline, and renin activity. The normotensive relatives of patients with essential hypertension did not differ in their responses from the normotensive subjects with no family history of hypertension, with the exception of plasma noradrenaline thirty minutes after nifedipine. These results provide evidence to suggest that there is no functional abnormality with increased dependency of vascular smooth muscle tone on calcium influx in the prehypertensive state.

It has been reported that patients with essential hypertension have high plasma prolactin levels and suggested that reduced central dopaminergic activity may be a factor in the pathogenesis of essential hypertension. This study examines the influence of posture on plasma prolactin, plasma catecholamines, plasma renin activity, blood pressure and heart rate in 24 patients with borderline hypertension (age 19 +/- 1 years) and 20 normotensive subjects matched for age and body mass index. Supine plasma prolactin levels were similar in both groups [borderline hypertension, 11.3 +/- 0.7 ng/ml; normotensive, 10.7 +/- 0.8 ng/ml (mean +/- s.e.m.)] and no increase in plasma prolactin was observed after 10 min standing in both groups. Normotensive and borderline hypertensive subjects had similar values for supine and upright plasma renin activity and plasma norepinephrine. There were no significant correlations between supine plasma prolactin and supine blood pressure, supine plasma renin activity or plasma norepinephrine when data from both normotensive and borderline hypertensive subjects were combined. These results may provide indirect evidence against the occurrence of reduced central dopaminergic activity in borderline hypertension.

To define the role of the renal dopaminergic system in the pathogenesis of essential hypertension, urinary free dopamine excretion was examined in 23 normotensive subjects who had one or more first-degree relatives with essential hypertension, and also in 36 matched control subjects without any such family history. The group urinary dopamine excretion and urinary sodium excretion were not different. However, a significant urine dopamine-sodium relationship was apparent in the controls but not in the relatives due to relatively high dopamine output in those with lower sodium excretion. The two groups were similar as regards blood pressure (BP), plasma renin activity (PRA), prolactin and catecholamines. These findings demonstrate an alteration in the urine dopamine-sodium relationship in some normotensive subjects with genetic risk of hypertension.

Plasma and urine norepinephrine, epinephrine, plasma renin activity and aldosterone were measured in 11 young men (mean age, 21 years) with a high blood pressure in the clinic who maintained a high home blood pressure and 12 men with an elevated clinic blood pressure who had a normal home blood pressure. Plasma samples were drawn following 30 min rest in the clinic, and 24-hour urine samples were collected at home. The two groups of hypertensives could not be distinguished on the basis of clinic blood pressure, plasma norepinephrine, epinephrine, renin activity or aldosterone. Patients with a high home blood pressure were characterized by a high urinary norepinephrine excretion. These results suggest that the patients whose blood pressure remained elevated at home had an increased sympathetic nerve activity at home.