Abstract

1. The Ca(2+)-channel agonist, Bay K 8644, induced small contractions in aortae from Wistar-Kyoto (WKY) rats of 5-week-, 3-month-, 1-year- and 1.5-year-old, which were unaltered with age. These contractions were increased by partial depolarization with 15 mM K+. 2. In segments from spontaneously hypertensive rats (SHR), the contractions obtained in both situations were similar and equivalent to those observed in segments from normotensive animals partially depolarized. Responses to Bay K 8644 were modified by age only in tissues from the SHR, the responses to this agent in basal conditions being increased in tissues from 3-month- and 1-year-old animals and depressed in those from 1.5-year SHR. 3. A reduction of the response to Bay K 8644 was observed in partial depolarized endothelium denuded segments from WKY of all ages, and no modification in basal situation. However, the direct contractions induced by Bay K 8644 in aortae from 3-month- and 1.5-year-old SHR were reduced by endothelium removal. 4. These results suggest that: (a) in the hypertensive strain the voltage-gated Ca2+ channels seem to be partially activated; (b) the direct contractions induced by Bay K 8644 were unaltered by age in aortae from WKY but increased in tissues from SHR of 3-month-and-1-year old and depressed in those from 1.5 years, and (c) the contractions evoked by Bay K 8644 seem to involve an endothelium-derived contracting factor in aortae from both strains, or the endothelium produces a partial depolarization of vascular smooth muscle that increases the responsiveness to Bay K 8644.

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