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1. Blood pressure, blood volume and renal blood flow were determined in 101 men; forty-three were normal subjects and fifty-eight were untreated permanent essential hypertensive patients with normal renal function and equilibrated sodium balance. 2. A significant negative pressure-volume relationship was observed overall. The relationship could be expressed as a hyperbola whose slope expressed the reduction in blood volume per unit rise in pressure: the higher the blood pressure, the lower the slope. Thus essential hypertensive subjects have a smaller decrement in blood volume per unit rise in pressure than normal subjects. 3. The relation between change in blood volume and change in pressure was confirmed in each individual by defining for each a ration deltaV/deltaP, statistically identical with the hyperbolic slope dV/dP. The deltaV/deltaP ratio was found to be well correlated with the renal blood flow and the creatinine clearance. No correlation existed between the total blood volume and these two renal parameters. 4. It is concluded that the present study demonstrates a blood volume regulation disturbance in essential hypertension and provides evidence from human studies that a renal defect accompanies high blood pressure.
Clin Sci Mol Med 1976 Mar
PMID:The pressure-volume relationship in normotensive and permanent essential hypertensive patients. 94 74

1. In patients with mild or moderate essential hypertension, oral propranolol, given in incremental doses, produced a moderate but significant lowering of blood pressure which was correlated with the concentration of propranolol in plasma. 2. Propranolol also reduced plasma renin activity (PRA) in the supine posture, on standing and after intravenous frusemide. However, 'supine' and 'frusemide' PRA values were markedly reduced at a plasma concentration of propranolol that had little effect on blood pressure. 3. On administration of propranolol there was little correlation between blood pressure decrease and PRA suppression, and even less between pretreatment PRA values and hypotensive response. 4. It is concluded that in patients with mild and moderate hypertension and low or normal plasma renin activity, suppression of PRA is not an important determinant of the hypotensive response to propranolol.
Clin Sci Mol Med Suppl 1975 Jun
PMID:Hypotensive and renin-suppressing activities of propranolol in hypertensive patients. 105 79

1. Twenty-three subjects with essential hypertension were followed for a period of up to 7 years. They were untreated during the investigations. 2. Plasma renin concentration was found to decrease temporarily in some subjects. The ultimate change was a gradual rise. In those subjects who suffered myocardial infarction renin tended to rise more sharply. 3. A relationship was established with the rise in renal vascular resistance, which almost invariably occurred over the years.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Follow-up of renin in essential hypertension. 107

1. As experimental models of reduced nephron population in man, (a) twelve men aged 15-32 years who had one kidney removed 1-13 years previously and (b) fourteen normotensive men aged 70-90 years were studied. Results were compared with those in eighteen normotensive men aged 18-28 years and eleven men aged 19-33 years with essential hypertension. 2. While the subjects followed a routine of normal diet and daily activity, measurements were made, after overnight recumbency and in the fasting state, of plasma volume and renin activity on one occasion in hospital and of blood pressure on five to fourteen occasions in the home. Blood pressure was also measured after standing for 2 min and plasma renin activity after 1 h standing, sitting or walking. Twenty-four hour urinary aldosterone excretion was also measured. 3. The measurements were repeated in the normotensive subjects and subjects in (a) and (b) above after 10 days of sodium-restricted diet (40 mmol of sodium/day). 4. The mean plasma renin activity (recumbent) in essential hypertensive subjects was higher than in normotensive subjects. In subjects of (a) and (b) above, it was lower than normotensive subjects, and was not increased by dietary sodium restriction in subjects of (a). 5. The mean aldosterone excretion level was lower in old normotensive subjects than in the other groups, and increased in each group after dietary sodium restriction. 6. Mean plasma volume/surface area was not different between the four groups and in normotensive, essential hypertensive and nephrectomized subjects but not subjects aged 70-90 years was negatively correlated with standing diastolic blood pressure.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Solitary kidney and ageing as causes of low renin and aldosterone concentrations: relevance to "low-renin" essential hypertension. 107 1

1. Patients with mild essential hypertension and elevated plasma renin activity, when compared with normal subjects and hypertensive subjects with normal plasma renin, demonstrated features of sympathetic nervous cardiovascular excitation, accompanied by a raised plasma noradrenaline concentration. 2. An elevated heart rate at rest, shortened cardiac pre-ejection period, and greater heart rate reduction with acute beta-adrenoreceptor blockade (intravenous propranolol) in high-renin essential hypertension were indicative of adrenergic cardiac excitation. An elevated total of peripheral vascular resistance at rest and a greater fall in peripheral resistance with alpha-adrenoreceptor blockade (intravenous phentolamine) suggested the existence of a neurogenic increase in arteriolar resistance. 3. Blood pressure was normalized by 'total' autonomic blockade (atropine plus propranolol plus phentolamine) in the hypertensive subjects with elevated plasma renin activity. 4. These findings suggest that in mild high-renin essential hypertension increased adrenergic drive to the heart and resistance vessels exists. The elevation of blood pressure is sustained predominantly by neurogenic mechanisms. The high plasma renin activity is seen as an expression of sympathetic nervous system overactivity.
Clin Sci Mol Med Suppl 1976 Dec
PMID:High-renin essential hypertension: adrenergic cardiovascular correlates. 107 2

1. Supine plasma renin activity and its responsiveness to erect posture and frusemide were reduced in fifty-one patients with essential hypertension, compared with fifty-one age- and sex-matched control subjects. 2. Twenty-four hour urinary sodium excretion was similar in hypertensive patients nad control subjects. 2. Twenty-four hour urinary sodium excretion was similar in hypertensive patients and control subjects, but after intravenous frusemide hypertensive patients excreted significantly less sodium. 3. A significant inverse relationship between plasma renin activity and diastolic blood pressure was demonstrated in hypertensive patients and in normotensive control subjects. 4. A significant inverse relationship between plasma renin activity and age, independent of blood pressure, was shown in hypertensive patients and control subjects. 5. It is concluded that the reduced renin values found in essential hypertension are, in part, the result of the elevated blood pressure acting on the kidney.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Reduced plasma renin activity in essential hypertension: effects of blood pressure, age and sodium. 107 3

1. Saralasin (Sar1-Ala8-angiotensin II), a competitive inhibitor of angiotensin II (AII), has been infused into normal subjects and patients with essential hypertension when deprived of sodium by 5 days of a 10 mmol/day sodium diet. 2. When saralasin was given by an incremental rate of infusion starting at 0-25 microng min-1 kg-1, sodium-deprived normal subjects showed a fall in standing blood pressure with no change in lying blood pressure, sodium-deprived normal-renin hypertensive patients showed no change in lying or standing blood pressure and sodium-deprived low-renin patients showed a significant sustained rise in lying and standing blood pressure. 3. These findings suggest that: (a) standing blood pressure in sodium-deprived normal subjects is angiotensin II dependent; (b)normal-renin hypertensive patients when sodium deprived by diet alone do not appear to be angiotensin II dependent (angiotensin II is unlikely therefore to be directly maintaining their blood pressure on their normal sodium intake);(c) the rise in blood pressure seen in low-renin hypertensive patients with saralasin may be a further way of distinguishing this group of patients.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Angiotensin II blockade in normal subjects and essential hypertensive patients. 107 6

1. In all three renin sub-groups of essential hypertension, the state of sodium balance determines the degree of participation of the renin-angiotensin system in sustaining high blood pressure. 2. Even the low-renin type can become renin-dependent when sufficient sodium depletion has bee achieved. 3. The main difference between patients of these sub-groups appears to be their variable capacity to become depleted of sodium under standard dietary regimens.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Determination of renin-dependency and sodium-dependency in the three renin sub-groups of essential hypertension. 107 7

1. Plasma renin activity and circulating amounts of blood angiotensin II were measured in twenty-six patients with uncomplicated essential hypertension. 2. Measurements were made during a control period and at 1, 4, 9 and 14 weeks of diuretic treatment with metolazone or hydrochlorothiazide. 3. Linear regression analysis indicated a progressive change in the relation of plasma renin activity and blood angiotensin II. 4. During chronic diuretic therapy (beyond 14 weeks) blood angiotensin II had stabilized to low and relatively fixed values across a wide range of plasma renin activities.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Dissociation of blood angiotensin II and plasma renin activity during chronic treatment in essential hypertension. 107 8

1. Analysis of relationships between blood volume, vascular capacitance, cardiopulmonary and peripheral blood volumes, labelled albumin disappearance rate, plasma renin activity, blood pressure and age was performed in essential hypertensive males. 2. The results indicate that capacitance bed constriction probably occurs with age in essential hypertension leading to an increase in the product blood volume xvascular capacitance tone even in the presence of low blood volume. 3. A metabolic defect in the venous vascular bed along with an abnormality of regulation of renal sodium excretion is postulated.
Clin Sci Mol Med Suppl 1976 Dec
PMID:The role of vascular capacitance in the genesis of essential hypertension. 107 9


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