Abstract
Enhanced contractile responsiveness to the calcium channel agonist Bay K 8644 has been documented in large conduit arteries and small muscular arteries from hypertensive rats. The present study examined the effects of Bay K 8644 on the intracellular calcium concentration ([Ca2+]i) in microvessels from stroke-prone spontaneously hypertensive rats and normotensive Wistar-Kyoto rats. Using microspectrofluorometry of fura-2, [Ca2+]i was measured in smooth muscle cells localized on arteriolar fragments (15-35 μm external diameter) isolated after collagenase digestion of the pancreas. Resting [Ca2+]i in hypertensive arterioles (94±6 nM, n=29) did not differ from that in normotensive vessels (81±4 nM, n=40). KCl (50 mM), applied alone and in the presence of Bay K 8644 (30 nM), stimulated increases in [Ca2+]i that were reversed in calcium-free solution and with nifedipine (10 μM), consistent with activation of potential-operated calcium channels. Potassium-induced calcium transients were consistently potentiated by Bay K 8644. The change in [Ca2+]i evoked by KCI alone or in combination with Bay K 8644 did not differ between arterioles from hypertensive and normotensive rats. In 24% of the vessels from hypertensive rats and in 29% of those from normotensive rats, Bay K 8644 evoked an increase in [Ca2+]i that did not differ significantly between the two strains. The findings indicate that, in contrast to observations made in larger arteries, there is no evidence of a functional abnormality in potentialoperated calcium channels in very small arterioles from genetically hypertensive rats.
Original language | English (US) |
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Pages (from-to) | 380-388 |
Number of pages | 9 |
Journal | Hypertension |
Volume | 20 |
Issue number | 3 |
DOIs | |
State | Published - Sep 1992 |
Externally published | Yes |
Keywords
- Arterioles
- Bay K 8644
- Calcium channels
- Muscle, smooth, vascular
- Nifedipine
- Rats, inbred SHR
ASJC Scopus subject areas
- Internal Medicine