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Unexpected pressor responses to propranolol in essential hypertension. An interaction between renin, aldosterone and
Insights
Propranolol effectively lowers blood pressure in most hypertension patients. However, some experience no change or even a rise in blood pressure, linked to renin-aldosterone system and alpha-sympathetic activity.
Area of Science:
- Cardiology
- Pharmacology
- Hypertension Research
Background:
- Benign essential hypertension affects a significant portion of the population.
- Propranolol is a beta-blocker commonly used in hypertension management.
- Individual responses to propranolol can vary, necessitating further investigation.
Purpose of the Study:
- To retrospectively analyze blood pressure responses to propranolol in hypertensive patients.
- To investigate factors influencing variable patient responses to propranolol treatment.
- To explore the relationship between propranolol, the renin-aldosterone system, and sympathetic activity.
Main Methods:
- Retrospective analysis of 187 patients with benign essential hypertension treated with propranolol.
- Categorization of patients into responders, non-responders, and pressor-responders based on blood pressure changes.
- Comparison of clinical characteristics, pulse rate reduction, pretreatment renin values, and plasma renin activity/aldosterone excretion.
Main Results:
- 54% of patients showed decreased blood pressure (responders), 35% had no significant change (non-responders), and 11% experienced increased blood pressure (pressor-responders).
- All groups showed similar pulse rate reduction, indicating comparable beta-blockade.
- Responders had higher pretreatment renin and greater decreases in renin and aldosterone; pressor-responders showed minimal hormonal changes and increased body weight.
Conclusions:
- Varied blood pressure responses to propranolol may stem from interactions between renin-aldosterone suppression and alpha-sympathetic activity.
- Pressor responses in some patients could be due to unopposed alpha-tone, lack of hormonal suppression, and fluid retention.
- Propranolol's hypotensive effect in responders is likely mediated by renin suppression, counteracting alpha-sympathetic tone and limiting aldosterone-driven sodium retention.
Abstract:
The blood pressure response to propranolol treatment was analyzed retrospectively in 187 patients with benign essential hypertension. In most patients (102 patients, 54 per cent) systolic and/or diastolic blood pressure was decreased by more than 10 per cent (responders). No significant change in blood pressure occurred in 35 per cent (65 patients) of the patients (nonresponders). Surprisingly, in 20 patients (11 per cent) systolic (8 patients) and/or diastolic (14 patients) blood pressure was increased by more than 7 per cent (pressor-responders). All three subgroups received similar amounts of propranolol and irrespective of the effect on the blood pressure, propranolol produced a similar reduction in pulse rates, suggesting similar degree of beta blockade. The three subgroups did not differ in their clinical characteristics, except that the nonresponders were significantly older than the responders. Pretreatment renin values were highest in the responders, somewhat lower in the nonresponders and significantly lower in the pressor-responders. In a representative subset of 66 patients, control and treatment values for plasma renin activity and aldosterone excretion were compared. The responders had the most pronounced decreases in both renin and aldosterone. In striking contrast, no significant changes were observed in the two hormones in those patients whose blood pressure levels rose. Moreover, in the pressor-responders, the drug produced the greatest increases in body weight, reflecting sodium retention. The differences in blood pressure responses observed in different patients may be explained by various interplays between the drug-induced suppression of renin and aldosterone, and the operation of unapposed or reactive alpha sympathetic activity. The latter is presumably active in all patients tending to cause vasoconstriction and hence an increase in peripheral resistance. In the pressor-responders such unopposed alpha-tone combined with the demonstrated lack of renin and aldosterone suppression with attendant fluid retention could work to produce the paradoxical pressor responses. In contrast, in those whose blood pressure levels drop, the drug-induced suppression of renin leads to decreased peripheral resistance despite the unopposed alphatone. The accompanying decrease in aldosterone limits sodium retention and contributes to the fall in blood pressure levels.