Propranolol therapy in essential hypertension

1. Indomethacin was administered alone or in addition to either diuretic or propranolol therapy to three groups of patients with essential hypertension on a free sodium diet. 2. Indomethacin administration reduced renin secretion by about 30% in untreated uncomplicated hypertensive patients and by about 75% in those whose renin secretion had either been stimulated or suppressed by maintained diuretic or β-adrenoreceptor-blockade therapy. 3. Indomethacin administration produced no net effect on blood pressure in untreated patients with uncomplicated hypertension but it blunted or reversed the antihypertensive effect of either diuretic or propranolol therapy. 4. Salt and water retention may be an important factor in the blood pressure-raising effect of indomethacin during diuretic or propranolol therapy: In addition, prostaglandin synthesis may be important in counteracting increased α-adrenergic tone, which may limit the blood pressure-lowering effect of β-adrenoreceptor-blockade. 5. Because of these interactions and their pressor potential indomethacin should be used with caution when combined with either diuretics or β-adrenoreceptor blockers.

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Decrease in α-Adrenoceptor-Mediated Vasoconstriction Parallels the Antihypertensive Response to Propranolol in Patients with Normal Renin Essential Hypertension

Clinical Science ◽

10.1042/cs061445s ◽

1981 ◽

Vol 61 (s7) ◽

pp. 445s-448s ◽

Cited By ~ 3

Author(s):

F. W. Amann ◽

P. Bolli ◽

L. Hulthén ◽

W. Kiowski ◽

F. R. Bühler

Keyword(s):

Essential Hypertension ◽

Plasma Renin Activity ◽

Forearm Blood Flow ◽

Plasma Renin ◽

Renin Activity ◽

Plasma Adrenaline ◽

Before And After ◽

Β Receptor ◽

Antihypertensive Response ◽

Propranolol Therapy

1. α1-Adrenoceptor-mediated vasoconstriction was studied before and during propranolol therapy in eight normal renin essential hypertensive patients; four were known ‘responders’ and four, age-matched ‘non-responders’ to previous β-receptor blocker monotherapy. Plasma renin activity, plasma adrenaline and noradrenaline concentrations as well as forearm blood flow were measured before and during regional postjunctional α1-adrenoceptor blockade with prazosin. All measurements were done on placebo and again after 6 weeks’ propranolol monotherapy (320 mg/day). 2. Propranolol reduced heart rate and plasma renin activity to the same extent in ‘responders’ and ‘non-responders’. Resting plasma adrenaline concentrations tended to be higher in ‘responders’ before propranolol; they remained unchanged in both groups on propranolol. Plasma noradrenaline concentrations were similar in both groups before and on propranolol. 3. Before propranolol forearm flow was not different in ‘responders’ and ‘non-responders’. Non-specific vasodilatation with sodium nitroprusside produced a similar increase in forearm flow before and after propranolol in both groups. 4. Prazosin-induced increments in forearm flow tended to be higher in ‘responders’ before propranolol. After propranolol the vasodilator effect of prazosin was attenuated in ‘responders’ but it remained unchanged in ‘non-responders’ (P < 0.01). 5. In patients with normal renin essential hypertension the antihypertensive response to propranolol monotherapy is paralleled by a decrease in postjunctional α1-adrenoceptor-mediated vasoconstriction.

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Abnormal renal haemodynamics during exercise in young patients with mild essential hypertension without treatment and during long-term propranolol therapy

Scandinavian Journal of Clinical and Laboratory Investigation ◽

10.3109/00365517809108821 ◽

1978 ◽

Vol 38 (6) ◽

pp. 567-571 ◽

Cited By ~ 6

Author(s):

E. B. Pedersen

Keyword(s):

Essential Hypertension ◽

Young Patients ◽

Renal Haemodynamics ◽

Propranolol Therapy

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Comparison between short-term Renal Haemodynamic Effects of Propranolol and Nadolol in Essential Hypertension: A Crossover Study

Clinical Science ◽

10.1042/cs0670243 ◽

1984 ◽

Vol 67 (2) ◽

pp. 243-248 ◽

Cited By ~ 12

Author(s):

Boothur J. Z. Danesh ◽

Joyce Brunton ◽

David J. Sumner

Keyword(s):

Essential Hypertension ◽

Renal Plasma Flow ◽

Haemodynamic Effects ◽

Term Therapy ◽

Second Phase ◽

Short Term ◽

Carry Over ◽

Renal Vascular ◽

Single Blind ◽

Propranolol Therapy

1. The effect of 4-6 weeks’ treatment with propranolol and nadolol on effective renal plasma flow (ERPF) and glomerular filtration rate (GFR) was studied, in 14 patients with essential hypertension, in single blind, random and cross-over design. 2. Both drugs caused comparable effective lowering of pulse and blood pressure. 3. When taken as the first drug, propranolol caused significant reduction in ERPF and GFR and a rise in filtration fraction (FF) and renal vascular resistance (RVR), whereas nadolol caused distinct rise in ERPF and a fall in FF and RVR but GFR remained unchanged. 4. These haemodynamic effects were reduced when propranolol was given immediately after the withdrawal of nadolol and were obviated when nadolol followed propranolol therapy. This suggested a carry-over effect of the first drug into the second phase of treatment. 5. We conclude that with short term therapy in essential hypertension, propranolol has a renal vasoconstrictor and nadolol a vasodilator effect.

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Effect of Propranolol Therapy on Aldosterone Responses to Angiotensin II and Adrenocorticotropic Hormone in Essential Hypertension

Clinical Science ◽

10.1042/cs0610107 ◽

1981 ◽

Vol 61 (1) ◽

pp. 107-110 ◽

Cited By ~ 4

Author(s):

M. S. Golub ◽

M. L. Tuck ◽

D. B. Fittingoff

Keyword(s):

Essential Hypertension ◽

Angiotensin Ii ◽

Plasma Renin Activity ◽

Plasma Cortisol ◽

Adrenocorticotropic Hormone ◽

Plasma Renin ◽

Plasma Aldosterone ◽

Renin Activity ◽

Before And After ◽

Propranolol Therapy

1. The plasma aldosterone responses to exogenous angiotensin II and adrenocorticotropic hormone (ACTH) were studied before and after 1 month of propranolol therapy (120–240 mg/day) in eight patients with essential hypertension. 2. Basal supine plasma renin activity was decreased (P < 0.001) after propranolol, whereas plasma aldosterone was unchanged. After 3 h of upright posture the increases in both plasma renin activity and aldosterone were decreased (P < 0.05) after propranolol. 3. Plasma aldosterone responses to exogenous angiotensin II and ACTH were not significantly different after propranolol. Serum and urinary electrolytes and plasma cortisol were also unaffected by propranolol therapy. 4. It is concluded that changes in adrenal sensitivity are not responsible for maintaining unchanged supine plasma aldosterone concentrations after β-adrenoceptor antagonism in essential hypertension.

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