{'fraction_non_alphanumeric': 0.05561797752808989, 'fraction_numerical': 0.042134831460674156, 'mean_word_length': 4.496913580246914, '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}}
Voltage-Dependent Ca 21 Channels in Resistance Arteries From Spontaneously Hypertensive Rats

Alterations in voltage-dependent Ca 2+ channels in the arterial smooth muscle cells of spontaneously hypertensive rats (SHR) were investigated using the whole-cell voltage clamp and compared with Wistar-Kyoto (WKY) rats. Single cells were freshly isolated from resistance mesenteric arteries from 4to 5-week-old (young) and 16to 18-week-old (adult) SHR. Elevated blood pressure was only evident in adult SHR, not in young SHR. In young rats, the Ca2+ channel current density (current amplitude normalized by cell capacitance) was significantly higher (P<.01) in SHR than in WKY rats at the command potential of -10 mV or higher (with 50 mmol/L Ba2+): The current density at 20 mV was -16.8+1.1 pA/pF in SHR (n=38 cells) and -11.0±0.8 pA/pF inWKY rats (n=30 cells). In adult rats, the difference in current densities disappeared: -15.9+1.3 pA/pF in SHR (n=25 cells) and -15.6+1.5 pA/pF in WKY rats (n=29 cells). The ratio of maximal amplitude of T-type current to that of L-type current was low in young SHR (0.10+0.01) compared with the other three groups (0.16 to 0.20). Neither the activation curve nor the steady-state inactivation curve of SHR was different from that of age-matched WKY rats. However, the activation curves in adult rats were shifted to a hyperpolarized direction compared with those of young rats in both strains. These results suggest that the increased activity of voltage-dependent L-type Ca21 channels of resistance arteries in young SHR may be related to the development of hypertension. The changes observed in adult rats may be due to a secondary modification of the channel during maturation and the presence of hypertension. (Circ Res. 1993;73:1090-1099.)