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Agonist-mediated changes in intracellular pH: role in vascular smooth muscle cell function
B C Berk1, M Canessa, G Vallega
1Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts.
Journal of Cardiovascular Pharmacology
|January 1, 1988
Summary
Intracellular pH (pHi) changes regulate vascular smooth muscle cell (VSMC) function. Agonists like angiotensin II alter pHi, impacting calcium mobilization and cell growth, suggesting pHi
Area of Science:
- Vascular Biology
- Cell Physiology
- Biochemistry
Background:
- Intracellular pH (pHi) is crucial for vascular smooth muscle cell (VSMC) function, influencing contractile tone.
- Limited understanding exists regarding agonist-induced pHi shifts and their broader roles in VSMC responses.
Purpose of the Study:
- Investigate agonist-mediated alterations in VSMC pHi.
- Elucidate the role of pHi in VSMC signal transduction, excitation-response coupling, and growth.
Main Methods:
- Utilized the pH-sensitive dye BCECF to measure pHi in cultured rat aortic VSMC.
- Analyzed pHi recovery mechanisms, specifically the Na+/H+ exchanger.
- Quantified intracellular Ca2+ mobilization and 45Ca2+ efflux in response to agonists.
Main Results:
- Basal pHi measured at 7.08 (suspended) and 7.26 (attached) VSMC.
- Angiotensin II and PDGF induced transient acidification followed by sustained alkalinization, linked to Ca2+ and Na+/H+ exchange.
- EGF and phorbol esters caused sustained alkalinization.
- Spontaneously hypertensive rat VSMC exhibited increased growth and Na+/H+ exchange compared to Wistar-Kyoto controls.
Conclusions:
- Agonist-induced pHi changes, particularly alkalinization, are critical for VSMC functions including signal transduction and growth.
- The Na+/H+ exchanger plays a key role in mediating pHi recovery and is implicated in VSMC hypertrophy/proliferation.
- Dysregulation of pHi may contribute to vascular diseases like hypertension.