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Biomedical subjects

P Weidmann

Publications and source records attributed to P Weidmann.

At least 145 records · Page 8Linked to original sources
PubMed1986

Body sodium/blood volume state in normotensive members of normotensive and hypertensive families.

Exchangeable sodium is lower than normal in young male patients with essential hypertension. This may reflect a primary abnormality of sodium metabolism, or natriuresis caused by sodium-independent elevation of arterial pressure. To investigate this question, 31 normotensive men with positive and 31 normotensive men with negative family history of essential hypertension were studied. Blood pressure tended to be higher in the former (121/78 +/- 9/8 (s.d.) versus 113/74 +/- 11/9 mmHg; P less than 0.005); mean age, urinary sodium or potassium excretion, plasma sodium, potassium, renin activity or aldosterone levels and creatinine clearance were comparable. Exchangeable sodium and blood volume were also similar in the two groups, when expressed in absolute values (3113 +/- 306 versus 3044 +/- 242 mmol and 4902 +/- 581 versus 4769 +/- 579 ml, respectively) or in relation to body surface area (100.8 +/- 7.1 versus 100.2 +/- 6% and 103.8 +/- 12.2 versus 102 +/- 11.3%). In both groups, exchangeable sodium and blood volume were unrelated to arterial pressure. The body sodium/blood volume state is normal in normotensive subjects with positive family history. The low exchangeable sodium of young patients with essential hypertension does not appear to reflect a primary familial abnormality of body sodium metabolism.

Aldosterone↗
PubMed1986

Plasma arginine-vasopressin levels during infusion of synthetic atrial natriuretic peptide on different sodium intakes in man.

The mechanisms involved in the diuretic action of the recently discovered group of atrial natriuretic peptides (ANP) are not entirely clear. To determine whether the diuresis and the changes in blood pressure produced by alpha-human ANP (alpha-hANP) involved a concomitant modification of circulating arginine-vasopressin (arg-VP), we evaluated the effects of synthetic alpha-hANP on plasma alpha-hANP, arg-VP, electrolytes, protein, haematocrit, blood pressure and urinary sodium and water excretion in 10 normal subjects on daily sodium intakes of 16, 140 and 310 mmol, respectively. Plasma alpha-hANP levels before and during a 45-min alpha-hANP infusion (0.09 micrograms/kg per min) tended to be slightly, though not significantly, higher on 'normal' or high sodium intake than on low sodium intake. Alpha-human ANP produced a fall in diastolic blood pressure (P less than 0.001) and to a lesser extent mean blood pressure, and a rise in heart rate (P less than 0.001) at all levels of sodium intake. The induction of diuresis, natriuresis and plasma volume contraction caused by alpha-hANP was greater on a high sodium intake than on 'normal' or low sodium intakes (P less than 0.001). Plasma arg-VP concentrations were lower (P less than 0.05) on a high than on a low sodium intake, but were not altered by an alpha-hANP infusion. The data indicate that in healthy humans circulating arg-VP may tend to decrease in response to a high salt diet. However, marked changes in plasma alpha-hANP concentrations have, regardless of sodium intake, no relevant influence on circulating arg-VP.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Antihypertensive treatment with bopindolol alone or combined with a diuretic in general practice.

beta blockers are now well established as alternative first-line drugs for treating hypertension. Bopindolol is a new beta blocker with a long duration of action and antihypertensive properties at low dosage. To assess the blood pressure (BP) lowering effect and tolerance of bopindolol, 590 hypertensive patients with diastolic BP greater than or equal to 100 mm Hg (age 22-78 years; mean +/- SD, 51 +/- 10) were evaluated prospectively by a study group of 248 practicing physicians. Following discontinuation of previous antihypertensive drugs for 4 weeks and/or a 2-week placebo phase, bopindolol 1 mg/day was given for 12 weeks. Bopindolol dose was decreased to 0.5 mg/day if diastolic BP after 8 weeks was less than or equal to 85 mm Hg; chlorthalidone 12.5-25 mg/day was added if diastolic BP was greater than or equal to 95 mm Hg after 4 or 8 weeks of bopindolol monotherapy. Compared to placebo, BP was lowered (p less than 0.0001) by bopindolol monotherapy (n = 273) from 159/104 +/- 14/4 to 139/89 +/- 12/6 mm Hg, by combination treatment (n = 288) from 165/108 +/- 16/6 to 145/95 +/- 16/7 mm Hg. Diastolic BP was reduced to less than 95 mm Hg by bopindolol 0.5 or 1 mg/day in 241 patients, by combination treatment in 150 patients. Bopindolol-induced absolute or percentage decreases in systolic or diastolic BP correlated with pretreatment BP (r = 0.22-0.51, p less than 0.001), but not with age (r = -0.05 to 0.08).(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1986

Complications in percutaneous transluminal dilatation of renal arteries.

We propose a classification of the complications in renal artery percutaneous transluminal angioplasty (PTA) according to their severity and their direct or indirect relationship to PTA. Minor complications are reversible within the normal recovery period after PTA, while major complications are irreversible or reversible but necessitate extended hospitalization or surgery. The following complications are reported in the literature as being directly related to PTA: hemorrhage at the puncture site, hemorrhage from renal or access artery perforation or rupture, occlusive or nonocclusive dissection of the renal or access arteries, renal artery thrombosis, renal artery spasm or embolism leading to segmental renal infarction, peripheral artery embolisation, and balloon rupture complications. The indirectly related complications include transient or irreversible renal insufficiency, contrast media hypersensitivity, pressure-drop-related cerebral or myocardial ischemia, and anticoagulation-related hemorrhage infections. In our own series of 105 PTA in 80 patients, complications occurred in 11% of which 4% were major, 1% indirectly related to PTA leading to death. In the reports available, the rate of major complication ranges between 3 and 10%, and the death rate around 1%.

Adult↗
PubMed1986

Alpha 1-adrenergic blockade and cardiovascular pressor responses in essential hypertension.

The effects of selective alpha 1-adrenergic blockade with terazosin on blood pressure and cardiovascular pressor responsiveness were assessed in 17 subjects with mild to moderate essential hypertension (mean age, 48 +/- 2 [SEM] years). As compared with a 2-week placebo period, 8 weeks of terazosin treatment (mean dose, 10.5 +/- 1.7 mg/day) caused a fall of supine (from 153/103 +/- 3/2 to 143/96 +/- 4/2 mm Hg; p less than 0.025) and upright (from 145/106 +/- 4/2 to 131/94 +/- 5/3 mm Hg; p less than 0.01) arterial pressure; a marked blunting of cardiovascular pressor responsiveness to norepinephrine, as judged from the pressor dose (from 73 +/- 9 to 2156 +/- 496 ng/kg/min; p less than 0.02) and from the rightward shift (p less than 0.01) of the plasma concentration-blood pressure response curve; and a slight increase in plasma norepinephrine concentration (from 37.7 +/- 3.3 to 52.2 +/- 7.8 ng/dl; p less than 0.01). Heart rate, body weight, exchangeable sodium, blood volume, and norepinephrine plasma clearance; plasma epinephrine, renin, angiotensin II, and aldosterone levels; the relationships between angiotensin II-induced increases in arterial pressure or plasma aldosterone and the concomitant increments of plasma angiotensin II; and heart rate responsiveness to isoproterenol did not change significantly after terazosin treatment. These findings suggest that the fall of arterial pressure induced by selective alpha 1-adrenergic blockade in subjects with essential hypertension is associated with, and probably explained by, inhibition of alpha 1-mediated, noradrenergic-dependent vasoconstriction. alpha 1-Adrenergic receptor antagonism did not modify body sodium concentration, the adrenomedullary component of the sympathetic nervous system, angiotensin II levels, or beta-adrenergic dependent mechanisms.

Adrenergic alpha-Antagonists↗
PubMed1986

Blood levels and renal effects of atrial natriuretic peptide in normal man.

Since mammalian atria were recently found to contain vasoactive and natriuretic peptides, we investigated the following in normal humans: plasma human atrial natriuretic peptide concentrations, effective renal plasma flow (ERPF), glomerular filtration rate (GFR), urinary water and electrolyte excretion, blood pressure (BP), and catecholamine, antidiuretic hormone (ADH), angiotensin II, and aldosterone levels before, during, and after intravenous administration of the newly synthetized alpha-human atrial natriuretic peptide (alpha hANP). In 10 subjects alpha hANP given as an initial bolus of 50 micrograms followed by a 45-min maintenance infusion at 6.25 micrograms/min increased plasma alpha hANP from 58 +/- 12 to 625 +/- 87 (mean +/- SEM) pg/ml; caused an acute fall in diastolic BP (-12%, P less than 0.001) and a hemoconcentration (hematocrit +7%, P less than 0.01) not fully explained by a negative body fluid balance; increased GFR (+15%, P less than 0.05) despite unchanged or decreased ERPF (filtration fraction +37%, P less than 0.001); augmented (P less than 0.05- less than 0.001) urinary chloride (+317%), sodium (+224%), calcium (+158%), magnesium (+110%), phosphate excretion (+88%), and free water clearance (from -0.76 to +2.23 ml/min, P less than 0.001) with only little change in potassium excretion; and increased plasma norepinephrine (P less than 0.001) while plasma and urinary epinephrine and dopamine, and plasma ADH, angiotensin II, and aldosterone levels were unchanged. The magnitude and pattern of electrolyte and water excretion during alpha hANP infusion could not be accounted for by increased GFR alone. Therefore, in normal man, endogenous alpha hANP seems to circulate in blood. alpha hANP can cause a BP reduction and hemoconcentration which occur, at least in part, independently of diuresis and are accompanied by sympathetic activation. An increase in GFR that occurs in the presence of unchanged or even decreased total renal blood flow is an important but not sole mechanism of natriuresis and diuresis induced by alpha hANP in man.

Atrial Natriuretic Factor↗
PubMed1986

Plasma levels and cardiovascular, endocrine, and excretory effects of atrial natriuretic peptide during different sodium intakes in man.

Endogenous plasma concentrations of human atrial natriuretic peptide (alpha hANP) as well as effects of synthetic alpha hANP on some cardiovascular, endocrine, and renal excretory parameters were investigated in 10 normal subjects during sodium (Na+) intakes of 17, 140, and 310 mmol/day, respectively. Plasma hANP was slightly but not significantly higher after 5 days of normal or high sodium intake than after 5 days of low sodium intake [54 +/- 13, 46 +/- 8, and 37 +/- 5 (mean +/- SEM) pg/ml, respectively]. alpha hANP infused at 0.1 microgram/kg X min during all Na+ intakes produced a similar fall in diastolic blood pressure (P less than 0.001) and rise in heart rate (P less than 0.001), a comparable percent increase in plasma norepinephrine (P less than 0.001), and a reduction in plasma cortisol and aldosterone (P less than 0.01-0.001) despite raised renin activity (P less than 0.05-0.001) and unchanged plasma electrolytes. alpha hANP-induced plasma volume contraction, diuresis, and natriuresis were greater during high than low Na+ intake (P less than 0.01-0.001). Therefore, in normal man different Na+ intakes are accompanied by marked modifications in renal excretory responsiveness to alpha hANP. Regardless of sodium intake, alpha hANP can promote BP reduction and hemoconcentration, elicit reflex (?) sympathetic activation, and depress basal circulating aldosterone and cortisol levels in the face of an activated renin system.

Adult↗
PubMed1986

Depressor effects and release of atrial natriuretic peptide during norepinephrine or angiotensin II infusion in man.

Alpha-human atrial natriuretic peptide (alpha hANP) is the major circulating form of ANP in man. The potential of synthetic alpha hANP to antagonize the pressor action of norepinephrine (NE) or angiotensin II (AII) and a possible influence of NE or AII pressor infusions on circulating immunoreactive ANP (irANP) were investigated in 14 normal young subjects. After titration of doses to increase mean blood pressure by about 20 mm Hg, NE or AII was infused at a constant rate for 110 min. Mean blood pressure (BP) was similar during NE and AII infusions [109 +/- 4 (+/- SEM) and 108 +/- 3 mm Hg, respectively]. However, synthetic alpha hANP injected in stepwise increasing doses of 10, 40, and 75 micrograms caused significantly greater (P less than 0.001) BP reductions during NE infusion. alpha hANP lowered BP progressively from 147/91 +/- 5/3 to 136/70 +/- 5/3 mm Hg during NE infusion (P less than 0.001) and only minimally from 133/96 +/- 3/3 to 132/89 +/- 4/4 during AII infusion. Heart rate was elevated more (P less than 0.01) after alpha hANP injection during NE infusion. Endogenous plasma irANP increased significantly after 20 min of NE or AII pressor infusion (P less than 0.01 and P less than 0.05, respectively); this rise was more pronounced (P less than 0.05) during NE (from 25 +/- 2 to 80 +/- 20 pg/ml) than during AII (from 21 +/- 3 to 31 +/- 3 pg/ml) infusion. These findings suggest that alpha hANP interacted preferentially with noradrenergic as compared to angiotensinergic BP control. Conversely, for a given rise in BP, NE elicited a greater rise in circulating irANP.

Adult↗
PubMed1986

Cardiovascular, endocrine and renal effects of atrial natriuretic peptide in essential hypertension.

Plasma concentrations of human atrial natriuretic peptide (hANP) and effects of synthetic alpha-hANP on blood pressure (BP), on endocrine and metabolic variables, and on renal function were investigated in 10 patients with essential hypertension. Alpha-human atrial natriuretic peptide was given intravenously as a 50-micrograms bolus followed by a 45-min infusion at 0.1 microgram/kg per min. The following effects were observed: (1) a marked rise in plasma alpha-hANP, (2) a progressive fall in BP (from 181/127 to 165/109 mmHg) and plasma volume, (3) a probably baroreflex-mediated sympathetic activation, evidenced by raised heart rate and plasma norepinephrine levels, (4) an increase in serum free fatty acids and circulating insulin (+45%), (5) an enhanced diuresis (+770%) and excretion of sodium (+665%), chloride (+524%), phosphate (+518%), other electrolytes, amino acids and free water clearance, (6) biphasic responses in the glomerular filtration rate (GFR) and p-aminohippurate (PAH) clearance, with initial increases (+40 and 30%, respectively) followed by a rapid return to (GFR), or even a fall below (PAH clearance) control values, and (7) a marked rise in the filtration fraction. Plasma antidiuretic hormone and urinary prostaglandin E2, F2 alpha and dopamine levels were not modified during alpha-hANP infusion, while plasma renin increased. Discontinuation of alpha-hANP was followed by rises in plasma aldosterone, the aldosterone:renin ratio and cortisol. Compared with previously studied normal subjects, in the hypertensive patients alpha-hANP caused a distinctly greater diuresis and electrolyte excretion but lowered BP only slightly more. In essential hypertension, as in normal man, alpha-hANP circulates in the blood and may exert a wide spectrum of cardiovascular, metabolic, endocrine and renal actions.

Adult↗
PubMed1986

Plasma kinetics of synthetic alpha-human atrial natriuretic peptide in man.

Atrial natriuretic peptides (ANPs) circulate in the blood stream and may modulate the regulation of blood pressure, sodium-fluid volume state and renal function. In man, alpha-human ANP (alpha hANP) is probably the major circulating form of ANP. To evaluate its plasma kinetics, we studied in 7 healthy men plasma alpha hANP concentrations under basal conditions and at short intervals during and up to 40 min after discontinuation of a 45-min constant alpha hANP infusion at a rate of 0.1 microgram/min/kg. From basal levels averaging 75 +/- 18 pg/ml (mean +/- SEM), plasma alpha hANP concentrations increased to 1,185 +/- 321 and 1,117 +/- 175 pg/ml at 30 and 40 min during the alpha hANP infusion, respectively. After discontinuing the latter, plasma alpha hANP decreased rapidly, following first-order kinetics, with a plasma half-life of 3.2 +/- 0.4 min. This finding is in line with the brief effects of intravenously applied alpha hANP and suggests that this system may be designed for rapid minute-to-minute adjustments.

Adult↗
PubMed1986

Blood pressure regulation on low and high sodium diets in normotensive members of normotensive or hypertensive families.

In members of hypertensive families a high sodium intake may have a pressor effect. The mechanism mediating the sodium sensitivity is unclear. Blood pressure, exchangeable sodium, plasma levels of norepinephrine, epinephrine, renin and aldosterone, the pressor response to infused norepinephrine or angiotensin II and the urinary excretion of prostaglandin (PG) E2 and F2 alpha were measured after 7 days of low sodium diet (urinary sodium 13 +/- 10 s.d. mmol/24 h) and 7 days of high sodium intake (urinary sodium 268 +/- 97 mmol/24 h) in 10 normotensive men without and 13 men with family history of essential hypertension. After the low sodium phase, blood pressure, heart rate, exchangeable sodium, plasma levels of norepinephrine, epinephrine, renin and aldosterone, pressor doses of norepinephrine or angiotensin II and the urinary excretion of PGE2 or PGF2 alpha did not differ between the two groups. After the high sodium phase, blood pressure increased only in subjects with positive (P less than 0.05) but not in those with negative family history. In the two groups exchangeable sodium increased (P less than 0.05) and plasma levels of NE (-33% versus -32%), renin (-31% versus -27%) or aldosterone (-74% versus -61%) and pressor doses of NE (-55% versus -54%) or ANG II (-72% versus -44%) decreased by a comparable extent. Urinary PGE2 or PGF2 alpha were unchanged. These findings suggest that a high dietary sodium intake exerts a pressor effect in subjects with familial predisposition to essential hypertension. This pressor effect is not explained by an abnormal adaptation of body sodium, sympathetic activity, renin-angiotensin-aldosterone axis, cardiovascular pressor responsiveness and renal prostaglandin excretion to a high sodium diet.

Adult↗
PubMed1985

[Effective long-term treatment of primary hyperlipoproteinemias with bezafibrate].

Bezafibrate, a new hypolipidemic agent, was evaluated in a single blind, placebo-controlled study lasting 14 months to 3 years in 40 patients with primary hyperlipoproteinemia of various types (23 patients with type II, 15 with type IV and 2 with type V). Bezafibrate in a dose of 200 mg 3 times daily reduced total serum cholesterol by an average of 17% (p less than 0.001) in hyperlipoproteinemia type II and by 24% (p less than 0.001) in type IV or V, lowered serum triglycerides by 31% (p less than 0.001) in hyperlipoproteinemia type II and by 58% (p less than 0.001) in type IV or V, while high-density-lipoprotein-cholesterol was increased by 17% (p less than 0.001) in type II and by 36% (p less than 0.001) in type IV or V. The few side effects encountered were only mild and transient. These findings show that bezafibrate affords safe and effective long-term treatment of patients with hyperlipoproteinemia.

Adult↗
PubMed1985

Rapidly progressive glomerulonephritis accompanying Legionnaires' disease.

A rapidly progressive, crescentic glomerulonephritis with acute oliguric renal failure occurred simultaneously with legionnaires' disease (LD) in a 52-year-old man. The diagnosis of LD was based on a sixfold rise in indirect fluorescent antibody titer against Legionella pneumophila serogroup 4. Treatment with erythromycin lactobionate resulted in a clinical resolution of pulmonary manifestations. The impairment of kidney function, however, was progressive and within two weeks led to end-stage renal failure requiring regular hemodialysis. This observation suggests that LD may trigger severe acute glomerulonephritis.

Antibodies, Bacterial↗
PubMed1985

Effects of the dopaminergic agonist cianergoline on blood pressure, the renin-angiotensin-aldosterone axis and the sympathetic nervous system in patients with essential hypertension.

Cianergoline is a new dopaminergic agonist with a predominant cardiovascular action. Its effects on blood pressure, the renin-angiotensin-aldosterone axis, the sympathetic nervous system and lipid metabolism were assessed in 20 patients with benign essential hypertension. Cianergoline given in increasing doses for 4 weeks (maximum daily dose 12 +/- 2 mg (SD)) and placebo both caused a slight decrease in arterial pressure, (from 159/104 to 152/98 mm Hg and from 154/104 to 149/103 mm, respectively; difference not significant). Supine and upright plasma renin activity, plasma aldosterone, norepinephrine, epinephrine and dopamine levels, urinary catecholamine excretion rates as well as serum prolactin, low and high density cholesterol and triglyceride concentrations were not changed after cianergoline or placebo. Total serum cholesterol and triglyceride levels decreased significantly after placebo, but were unchanged after cianergoline. 3 out of 10 patients in the cianergoline group complained of nausea. The findings indicate that the new dopaminergic agonist cianergoline exerts only a mild blood pressure lowering effect in patients with essential hypertension and does not modify the release of prolactin, lipid metabolism or the basal activity or postural responsiveness of the renin-angiotensin-aldosterone axis and of the sympathetic nervous system.

Adult↗
PubMed1985

Renal handling of norepinephrine and epinephrine in the pig.

To investigate the renal handling of catecholamines in the pig, intravenous infusions of 51Cr-EDTA and PAH were performed in 7 animals, and samples for simultaneous measurement of norepinephrine (NE), epinephrine (E), 51Cr-EDTA and PAH were obtained through catheters placed into the aorta, left renal vein and both urethers. For both kidneys together, 51Cr-EDTA clearance [GFR] averaged 48 +/- 14 (+/- SD) ml/min (2.23 +/- 0.66 ml/kg/min). In the left kidney, GFR averaged 22 +/- 9 ml/min, arteriovenous PAH extraction 0.87 +/- 0.09, and calculated total renal plasma flow 91 +/- 30 ml/min. Plasma NE and E were lower in renal venous than arterial blood (P less than 0.005), extraction ratios averaging 0.36 and 0.77, respectively. NE excretion rate in final urine (8.9 +/- 4.3 ng/min) exceeded transrenal NE extraction rate (5.2 +/- 3.9 ng/min) by 3.7 +/- 4.4 ng/min. In contrast, urinary E excretion rate (2.9 +/- 2.0 ng/min) was slightly lower than transrenal E extraction rate (3.6 +/- 3.8 ng/min). These observations suggest that in pig kidneys, plasma PAH extraction rate and GFR related to body weight are quite similar to values in man. Three quarters of circulating E are extracted for the most part by tubular secretion, and the slightly smaller amount appearing in urine is consistent with some intrarenal metabolism. NE, presumably originating from intrarenal neuronal release and/or de novo production, is secreted into the urine.

Animals↗
PubMed1985

Body sodium-blood volume state, aldosterone, and cardiovascular responsiveness after calcium entry blockade with nifedipine.

Exchangeable sodium, blood volume, plasma norepinephrine (NE), epinephrine, renin and aldosterone levels, and pressor responses to infused NE or angiotensin II (AII) were assessed in ten patients with essential hypertension on placebo, following 6 to 8 weeks of calcium-antagonist nifedipine (NIF), 3 X 10 to 20 mg/day, and after 6 to 8 weeks on NIF combined with the diuretic chlorthalidone (CHLOR), 25 to 50 mg/day. Pressor effects of infused calcium also were evaluated on placebo and NIF. Supine blood pressure was decreased from 151/97 +/- 5/2 (SEM) to 132/88 +/- 6/2 mm Hg after NIF alone (P less than 0.05) and to 124/83 +/- 7/3 mm Hg after NIF + CHLOR (P less than 0.01). Body wt was increased from 72.7 to 73.9 kg on NIF alone (P less than 0.05), but decreased to 72.1 (P less than 0.05 compared with placebo) after adding CHLOR. Exchangeable sodium also rose from 2642 +/- 237 to 3360 +/- 266 mmoles on NIF (+ 27%; P less than 0.01) and returned to control values (2638 +/- 248 mmoles) after addition of CHLOR. Plasma volume was only slightly modified on NIF (from 2621 +/- 193 to 2751 +/- 160 ml; + 5%), but was reduced to 2232 +/- 231 ml on NIF + CHLOR (P less than 0.05). Responses of circulating aldosterone to AII were similarly diminished (P less than 0.01) during both conditions. Heart rate, supine and upright plasma renin, aldosterone and catecholamine levels, and pressor responses to NE, AII, or calcium were not consistently changed.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1985

Norepinephrine-related mechanism in hypertension accompanying renal failure.

UNLABELLED: Various blood pressure (BP)-regulating factors were assessed before and after 4 weeks of selective norepinephrine (NE) inhibition with the sympathetic neurone blocker, debrisoquine, in nine hypertensive, nine normotensive hemodialysis patients (HDP), and 11 normal subjects. On placebo, hypertensive HDP had an increased total blood volume (P less than 0.05) and exchangeable sodium (P less than 0.001), while both HDP groups had increased (P less than 0.05) plasma clearances of NE and angiotensin II (AII), and tended to have higher basal plasma NE, renin, and AII levels, and lower BP responses to NE or AII than normal subjects. Plasma epinephrine and the chronotropic dose of isoproterenol (CDI) did not differ significantly among groups. Debrisoquine lowered supine BP markedly in hypertensive HDP (on average from 181/107 to 148/88 mm Hg) and slightly in normotensive HDP (143/78 to 131/76 mm Hg), but not in normal subjects (116/74 to 120/79 mm Hg). In all groups, plasma NE, CDI, and NE pressor dose were reduced in parallel (by 35 to 75%; P less than 0.05 to less than 0.001), and the relation between stepwise increasing plasma NE and BP changes during NE infusion was commensurably displaced to the left (P less than 0.01). The remaining parameters were not changed consistently. CONCLUSION: HDP, as normal subjects, respond to decreased sympathetic outflow with increased alpha- and beta-receptor sensitivity. Hypertension in HDP depends strongly on a NE-related mechanism. The latter seems to complement renin-angiotensin, sodium and fluid volume in the pathogenesis of high BP.

Adult↗