Impaired potassium-induced dilation in hypertensive rat cerebral arteries does not reflect altered Na+,K(+)-ATPase dilation
| Autor: | W Halpern, J G McCarron |
|---|---|
| Rok vydání: | 1990 |
| Předmět: |
Male
medicine.medical_specialty Physiology Sodium Potassium Cerebral arteries chemistry.chemical_element Vasodilation Posterior cerebral artery Rats Inbred WKY Sodium Channels Rats Inbred SHR Internal medicine medicine.artery medicine Animals Na+/K+-ATPase business.industry Cerebral Arteries Pathophysiology Rats medicine.anatomical_structure Endocrinology chemistry Anesthesia Hypertension Sodium-Potassium-Exchanging ATPase Cardiology and Cardiovascular Medicine business Artery |
| Zdroj: | Circulation Research. 67:1035-1039 |
| ISSN: | 1524-4571 0009-7330 |
| Popis: | We have recently demonstrated that K(+)-induced dilation of cerebral resistance-sized vessels has two independent components, only one of which seemed sodium pump dependent. In our current investigation, potassium-induced dilation of spontaneous tone was compared in cerebral arteries from normotensive Wistar-Kyoto rats and age-matched stroke-prone spontaneously hypertensive rats. Branches of the posterior cerebral artery were cannulated and pressurized, and these vessels developed spontaneous tone. After a 5-minute period in K(+)-free physiological saline solution, K+ was increased in 1-mM increments to a final concentration of 15 mM. In the normotensive arteries, K+ concentrations between 0 and 5 mM K+ resulted in dilations that had a transient (sodium pump-dependent) component, and K+ concentrations in excess of 7 mM produced dilations that lacked a transient (sodium pump-independent) component. Similar branches from the hypertensive rat also responded with transient dilations to K+ (less than 5 mM), and these were significantly greater at 3 mM K+. However, the maintained dilations to K+ (greater than 7 mM), noted in preparations from Wistar-Kyoto rats, were absent in seven of eight preparations. Thus, the impaired dilations, in the hypertensive vessels, to K+ described here is a consequence of altered function of some sodium pump-independent component rather than altered Na+,K(+)-ATPase activity. |
| Databáze: | OpenAIRE |
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