Article ; Online: Involvement of BKCa and KV potassium channels in cAMP-induced vasodilatation: their insufficient function in genetic hypertension.
2014 Volume 63, Issue 3, Page(s) 275–285
Abstract: Spontaneously hypertensive rats (SHR) are characterized by enhanced sympathetic vasoconstriction, whereas their vasodilator mechanisms are relatively attenuated compared to their high BP. The objective of our in vivo study was to evaluate whether the ... ...
| Abstract | Spontaneously hypertensive rats (SHR) are characterized by enhanced sympathetic vasoconstriction, whereas their vasodilator mechanisms are relatively attenuated compared to their high BP. The objective of our in vivo study was to evaluate whether the impaired function of BKCa and/or KV channels is responsible for abnormal cAMP-induced vasodilatation in genetic hypertension. Using conscious SHR and normotensive WKY rats we have shown that under the basal conditions cAMP overproduction elicited by the infusion of beta-adrenoceptor agonist (isoprenaline) caused a more pronounced decrease of baseline blood pressure (BP) in SHR compared to WKY rats. Isoprenaline infusion prevented BP rises induced by acute NO synthase blockade in both strains and it also completely abolished the fully developed BP response to NO synthase blockade. These cAMP-induced vasodilator effects were diminished by the inhibition of either BKCa or KV channels in SHR but simultaneous blockade of both K(+) channel types was necessary in WKY rats. Under basal conditions, the vasodilator action of both K(+) channels was enhanced in SHR compared to WKY rats. However, the overall contribution of K(+) channels to cAMP-induced vasodilator mechanisms is insufficient in genetic hypertension since a concurrent activation of both K(+) channels by cAMP overproduction is necessary for the prevention of BP rise elicited by acute NO/cGMP deficiency in SHR. This might be caused by less effective activation of these K(+) channels by cAMP in SHR. In conclusion, K(+) channels seem to have higher activity in SHR, but their vasodilator action cannot match sufficiently the augmented vasoconstriction in this hypertensive strain. |
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| MeSH term(s) | Adrenergic beta-Agonists ; Animals ; Blood Pressure ; Cyclic AMP/metabolism ; Hypertension/genetics ; Hypertension/metabolism ; Hypertension/physiopathology ; Isoproterenol ; Large-Conductance Calcium-Activated Potassium Channel alpha Subunits/metabolism ; Male ; NG-Nitroarginine Methyl Ester ; Nitric Oxide Synthase/antagonists & inhibitors ; Potassium Channels, Voltage-Gated/metabolism ; Rats, Inbred SHR ; Rats, Inbred WKY ; Vascular Resistance ; Vasodilation |
| Chemical Substances | Adrenergic beta-Agonists ; Kcnma1 protein, rat ; Large-Conductance Calcium-Activated Potassium Channel alpha Subunits ; Potassium Channels, Voltage-Gated ; Cyclic AMP (E0399OZS9N) ; Nitric Oxide Synthase (EC 1.14.13.39) ; Isoproterenol (L628TT009W) ; NG-Nitroarginine Methyl Ester (V55S2QJN2X) |
| Language | English |
| Publishing date | 2014-01-08 |
| Publishing country | Czech Republic |
| Document type | Journal Article ; Research Support, Non-U.S. Gov't |
| ZDB-ID | 1073141-6 |
| ISSN | 1802-9973 ; 0369-9463 ; 0862-8408 |
| ISSN (online) | 1802-9973 |
| ISSN | 0369-9463 ; 0862-8408 |
| DOI | 10.33549/physiolres.932718 |
| Database | MEDical Literature Analysis and Retrieval System OnLINE |
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