{'fraction_non_alphanumeric': 0.03773584905660377, 'fraction_numerical': 0.01650943396226415, 'mean_word_length': 4.975352112676056, 'pattern_counts': {'":': 0, '<': 3, '<?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}}
Two α1-Adrenergic Receptor Subtypes Regulating the Vasopressor Response Have Differential Roles in Blood Pressure Regulation

To study the functional role of individual α1-adrenergic (AR) subtypes in blood pressure (BP) regulation, we used mice lacking the α1B-AR and/or α1D-AR with the same genetic background and further studied their hemodynamic and vasoconstrictive responses. Both the α1D-AR knockout and α1B-/α1D-AR double knockout mice, but not the α1B-AR knockout mice, had significantly (p < 0.05) lower levels of basal systolic and mean arterial BP than wild-type mice in nonanesthetized condition, and they showed no significant change in heart rate or in cardiac function, as assessed by echocardiogram. All mutants showed a significantly (p < 0.05) reduced catecholamine-induced pressor and vasoconstriction responses. It is noteworthy that the infusion of norepinephrine did not elicit any pressor response at all in α1B-/α1D-AR double knockout mice. In an attempt to further examine α1-AR subtype, which is involved in the genesis or maintenance of hypertension, BP after salt loading was monitored by tail-cuff readings and confirmed at the endpoint by direct intra-arterial recording. After salt loading, α1B-AR knockout mice developed a comparable level of hypertension to wild-type mice, whereas mice lacking α1D-AR had significantly (p < 0.05) attenuated BP and lower levels of circulating catecholamines. Our data indicated that α1B- and α1D-AR subtypes participate cooperatively in BP regulation; however, the deletion of the functional α1D-AR, not α1B-AR, leads to an antihypertensive effect. The study shows differential contributions of α1B- and α1D-ARs in BP regulation.