Closure of multiple types of K+ channels is necessary to induce changes in renal vascular resistance in vivo in rats
| Autor: | Niels-Henrik Holstein-Rathlou, Thomas Hartig Braunstein, Isaiah Giese, Charlotte Mehlin Sorensen, Max Salomonsson |
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| Rok vydání: | 2011 |
| Předmět: |
Male
medicine.medical_specialty Potassium Channels Nifedipine Physiology Clinical Biochemistry Apamin Muscle Smooth Vascular Membrane Potentials Renal Circulation Rats Sprague-Dawley Mice chemistry.chemical_compound Physiology (medical) Internal medicine Potassium Channel Blockers Animals Medicine Large-Conductance Calcium-Activated Potassium Channels Potassium Channels Inwardly Rectifying Mibefradil business.industry Hyperpolarization (biology) Angiotensin II Potassium channel Rats Mice Inbred C57BL Arterioles Endocrinology chemistry Vasoconstriction Renal blood flow Pinacidil Benzimidazoles Vascular Resistance Calcium Channels medicine.symptom business medicine.drug |
| Zdroj: | Pflügers Archiv - European Journal of Physiology. 462:655-667 |
| ISSN: | 1432-2013 0031-6768 |
| Popis: | Inhibition of K(+) channels might mediate renal vasoconstriction. As inhibition of a single type of K(+) channel caused minor or no renal vasoconstriction in vivo in rats, we hypothesized that several classes of K(+) channels must be blocked to elicit renal vasoconstriction. We measured renal blood flow (RBF) in vivo in anesthetized Sprague-Dawley rats. Test agents were infused directly into the renal artery to avoid systemic effects. Inhibition of BK(Ca) and K(ir) channels (with TEA and Ba(2+), respectively) caused small and transient reductions in RBF (to 93 ± 2% and 95 ± 1% of baseline, respectively). K(ATP), SK(Ca) or K(v) channel blockade (with glibenclamide, apamin and 4-aminopyridine, respectively) was without effect. However, a cocktail of all blockers caused a massive reduction of RBF (to 15 ± 10% of baseline). Nifedipine and mibefradil abolished and reduced, respectively, this RBF reduction. The effect of the cocktail of K(+) channel blockers was confirmed in mice using the isolated blood-perfused juxtamedullary nephron preparation. A cocktail of K(+) channel openers (K(+), NS309, NS1619 and pinacidil) had only a minor effect on baseline RBF in vivo in rats, but reduced the vasoconstriction induced by bolus injections of norepinephrine or angiotensin II (by 33 ± 5% and 60 ± 5%, respectively). Our results indicate that closure of numerous types of K(+) channels could participate in the mediation of agonist-induced renal vasoconstriction. Our results also suggest that renal vasoconstriction elicited by K(+) channel blockade is mediated by nifedipine-sensitive Ca(2+) channels and partly by mibefradil-sensitive Ca(2+) channels. |
| Databáze: | OpenAIRE |
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