{'fraction_non_alphanumeric': 0.04081632653061224, 'fraction_numerical': 0.026455026455026454, 'mean_word_length': 5.245283018867925, 'pattern_counts': {'":': 0, '<': 1, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Effect of beta adrenoceptor antagonists on baroreceptor reflex sensitivity in hypertension

High‐pressure baroreceptor reflex sensitivity (BRS) was estimated by measuring the reflex heart rate response to pharmacologic elevation olblood pressure (phenylephrine, 150 to 200 f.Lg intravenously) in 18 patients with essential hypertension on two occasions: after a 4‐wk placebo period and after 9 wk of incremental doses of oral timolol (20, 40, and 60 mg daily). On placebo, measurements were pelformed both before and after propranolol (0.2 mglkg intravenously). The level of cardiac vagal inhibition, estimated by the heart rate change alter atropine (0.04 mglkg intravenously), was similar on placebo and on timolol, thereby permitting comparisons of BRS. BRS on placebo (belore and after propranolol) correlated with BRS on timolol (r = 0.87 and 0.90, p < 0.001), attesting to the reproducibility of BRS measurements. BRS was unchanged by either short‐term (propranolol) or long‐term (timolof) beta adrenoceptor inhibition. Results were similar in responders (n = 10), whose mean arterial blood pressure on timolol fell by 10 mm Hg or more, and in nonresponders. The findings do not provide evidence for a change in gain of the baroreceptor reflex arc under conditions of short‐ or long‐term beta adrenoceptor inhibition.