Premium
SECONDARY SIGNALLING MECHANISMS IN ANGIOTENSIN II‐STIMULATED VASCULAR SMOOTH MUSCLE CELLS
Author(s) -
Griendling Kathy K.,
Berk Bradford C.,
Socorro Lilian,
Tsuda Terutaka,
Delafontaine Patrick,
Alexander R. Wayne
Publication year - 1988
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1988.tb01051.x
Subject(s) - vascular smooth muscle , angiotensin ii , chemistry , microbiology and biotechnology , signalling , endocrinology , signalling pathways , medicine , renin–angiotensin system , smooth muscle , signal transduction , biology , receptor , blood pressure
SUMMARY 1. Activation of vascular smooth muscle by angiotensin II results in the generation of two second messengers, inositol trisphosphate (IP 3 ) and diacylglycerol (DG). 2. IP 3 is responsible for mobilizing calcium from endoplasmic reticulum. This signal is transient, most likely serving to initiate calcium events leading to contraction, and is attenuated by activation of protein kinase C. 3. DG stimulates protein kinase C and ultimately Na + /H + exchange, leading to intracellular alkalinization. Accumulation of DG/activation of protein kinase C is sustained, and may be enhanced by concurrent intracellular alkalinization. The delay in induction of the sustained response appears to be related to cellular processing of the angiotensin II‐receptor complex. 4. Angiotensin II‐stimulated, phospholipase C‐mediated IP 3 formation is also modulated by a pertussis toxin‐insensitive guanine nucleotide regulatory protein. 5. The GTP binding protein, movement of the receptor‐ligand complex, and the signals generated by the two second messengers, IP 3 and DG, interact in a complex manner to cause an integrated response of vascular smooth muscle cells to angiotensin II stimulation.