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PubMed1991

Endothelin and increased contractility in adult rat ventricular myocytes. Role of intracellular alkalosis induced by activation of the protein kinase C-dependent Na(+)-H+ exchanger.

Endothelin, a 21-amino acid vasoactive peptide, is among the most potent positively inotropic agents yet described in mammalian heart. Having demonstrated that endothelin's inotropic effect is due, in part, to an apparent sensitization of cardiac myofilaments to intracellular calcium, we determined whether this could be due to a rise in intracellular pH (pHi). In isolated adult rat ventricular cells loaded with the H(+)-selective fluorescent probe BCECF, 100 pM endothelin increased contractile amplitude to 190 +/- 26% of baseline and pHi by 0.08 +/- 0.02 (n = 8), whereas 1 nM endothelin increased pHi by 0.13 +/- 0.03 with little further increase in contractility. Amiloride (10(-4)M) prevented the increase in pHi in response to endothelin and reduced the inotropic response by 45%, although the inotropic effect could be readily restored by subsequent NH4Cl-induced alkalinization. Similarly, inhibitors of protein kinase C (H-7 and sphingosine) diminished or abolished the rise in pHi after endothelin superfusion while causing a decline in its inotropic effect comparable with that observed with amiloride. Pretreatment with pertussis toxin, which we have demonstrated results in complete ADP-ribosylation of the alpha-subunits of Go and Gi GTP-binding proteins and abolition of endothelin's positive inotropic effect, only partially reduced the intracellular alkalinization induced by the peptide, suggesting a complex signal transduction mechanism. Thus, the positive inotropic action of endothelin is due in part to stimulation of the sarcolemmal Na(+)-H+ exchanger by a protein kinase C-mediated pathway, resulting in a rise in pHi and sensitization of cardiac myofilaments to intracellular Ca2+.

Alkalosis↗
PubMedDate not supplied

Effect of non-respiratory alkalosis on brain tissue and cerebral blood flow in rats with damaged blood-brain barrier.

Acute alterations in plasma bicarbonate concentration have minimal effects on intracerebral pH and cerebral blood flow, perhaps due to blood-brain barrier mechanisms. To test this hypothesis, the consequences of an acute rise in the plasma bicarbonate concentration were studied in anesthetized rats previously subjected to an acute pressure pulse in the carotid system with unilateral damage to the blood-brain barrier. In rats subjected to a "heavy" hypertensive insult, the hemisphere on the side of the lesion showed a lactic acidosis, edema, and a depression of cerebral blood flow. An increase in the plasma bicarbonate concentrations of 15--20 mEq/1 during 35 minutes provoked a marked rise in the total CO2 content of this hemisphere, and a further increase in the lactate concentration, but did not later the brain edema nor affect further the already very low cerebral blood flow. An increase in the lactate concentration and a decrease of cerebral blood flow in the "reference" hemisphere indicated that the lesion was not completely unilateral. In rats subjected to a "moderate" hypertensive insult the changes were less pronounced and statistically not significant for all the parameters. There results illustrate the importance of an intact blood-brain barrier for the maintenance of intracerebral pH in the face of acute alterations in plasma [HCO3]. The impaired cerebral blood flow after an acute hypertensive insult did not appear to be influenced by the intracerebral [HCO3].

Alkalosis↗