Modulation of angiotensin II coronary vasoconstriction by cardiac prostaglandin synthesis

Male Sprague-Dawley rats (140-180 g) were anesthetized with alpha-chloralose and urethan. The cremaster muscle with intact blood supply and neural innervation was suspended in a tissue bath containing a modified Krebs solution. With the use of television microscopy the luminal diameters of third-order arterioles (14-32 micron) were measured before and after adding angiotensin II (ANG II, bath concn 10(-6) M). The arterioles responded to ANG II with an initial, transient constriction followed by a more prolonged dilation to a diameter larger than the control diameter. Pretreating the muscle with [Sar1, Ile8]ANG II significantly attenuated both the arteriolar constriction and subsequent dilation induced by ANG II. Treatment of the cremaster muscle with mefenamic acid or indomethacin, inhibitors of prostaglandin synthesis, produced a significant reduction in the diameter of the arterioles and abolished the dilator phase of the arteriolar response to ANG II without preventing the ANG II-induced constriction. These results demonstrate that within the intact microcirculation, ANG II produces both an arteriolar constriction and a dilation that are mediated by specific ANG II receptors. The ANG II-induced dilation of the arterioles appears to be caused by increased prostaglandin synthesis and release.

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Swimming training prevents fat deposition and decreases angiotensin II-induced coronary vasoconstriction in ovariectomized rats

Peptides ◽

10.1016/j.peptides.2013.06.002 ◽

2013 ◽

Vol 47 ◽

pp. 29-35 ◽

Cited By ~ 8

Author(s):

Patrick Wander Endlich ◽

Erick Roberto Gonçalves Claudio ◽

Washington Luiz da Silva Gonçalves ◽

Sonia Alves Gouvêa ◽

Margareth Ribeiro Moysés ◽

...

Keyword(s):

Angiotensin Ii ◽

Fat Deposition ◽

Ovariectomized Rats ◽

Swimming Training ◽

Coronary Vasoconstriction

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Angiotensin II Stimulation of Renal Prostaglandin Synthesis Elevates Circulating Prostacyclin in the Dog

Journal of Cardiovascular Pharmacology ◽

10.1097/00005344-198009000-00015 ◽

1980 ◽

Vol 2 (5) ◽

pp. 667-678 ◽

Cited By ~ 36

Author(s):

R. J. Shebuski ◽

J. W. Aiken

Keyword(s):

Angiotensin Ii ◽

Prostaglandin Synthesis ◽

Stimulation Of

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Dietary protein increases plasma renin and reduces pressor reactivity to angiotensin II

AJP Renal Physiology ◽

10.1152/ajprenal.1986.251.1.f34 ◽

1986 ◽

Vol 251 (1) ◽

pp. F34-F39 ◽

Cited By ~ 5

Author(s):

M. S. Paller ◽

T. H. Hostetter

Keyword(s):

Angiotensin Ii ◽

Dietary Protein ◽

Pressor Response ◽

Renin Angiotensin System ◽

Chronic Administration ◽

Plasma Renin ◽

Prostaglandin Synthesis ◽

Plasma Aldosterone ◽

Ang Ii ◽

Inhibition Of Prostaglandin Synthesis

The effect of dietary protein on the renin-angiotensin system was studied in rats. Rats were fed isocaloric, 50% (high protein, HP), or 6% (low protein, LP) protein diets with identical electrolyte content for 10 days. Food intake and electrolyte excretion were equivalent on the two diets. Plasma renin activity (PRA) was higher in HP (10.0 +/- 2.5 vs. 3.5 +/- 0.5 ng ANG I . ml-1 . h-1, P less than 0.02) as was plasma aldosterone. However, in conscious rats mean arterial pressure (MAP) was not different between groups. The pressor response to graded doses of angiotensin II (ANG II) was diminished by 30-60% with HP (all doses, P less than 0.05). ANG II binding by mesenteric artery smooth muscle particles did not differ between HP and LP. Chronic administration of captopril did not normalize the pressor response in HP. Urinary prostaglandin (PG) E and 6-keto-PGF1 alpha excretion was markedly increased by the HP diet. Acute inhibition of prostaglandin synthesis with meclofenamate restored the pressor response to ANG II in HP to that in LP. In summary, a HP diet increased PRA, plasma aldosterone, urinary PGE, and 6-keto-PGF1 alpha and decreased pressor responsiveness to ANG II. Resistance to ANG II was not reversed by chronic converting enzyme inhibition but was abolished by inhibition of prostaglandin synthesis.

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Prostaglandin synthesis by isolated rat glomeruli: effect of angiotensin II

AJP Renal Physiology ◽

10.1152/ajprenal.1980.239.5.f486 ◽

1980 ◽

Vol 239 (5) ◽

pp. F486-F495 ◽

Cited By ~ 3

Author(s):

D. Schlondorff ◽

S. Roczniak ◽

J. A. Satriano ◽

V. W. Folkert

Keyword(s):

Blood Flow ◽

Angiotensin Ii ◽

Glomerular Filtration ◽

Renal Blood Flow ◽

Prostaglandin Synthesis ◽

Breakdown Product ◽

Isolated Glomeruli ◽

Isolated Rat

Prostaglandins play a role in the regulation of renal blood flow and glomerular filtration. In the presence of [14C]arachidonate the pattern of prostaglandins produced by isolated glomeruli was PGF2 alpha > PGE2 > PGD2 = TXB2 = 6-keto-PGF1 alpha (a metabolite of prostacyclin). Glomeruli prelabeled with [14C]arachidonate showed an additional labeled prostaglandin that co-chromatographs with 6,15-diketo-13,13-dihydro-PGF1 alpha and may represent breakdown product of prostacyclin. Thus, prostacyclin, judged by its breakdown products, was the second most abundant prostaglandin produced. These results were confirmed by specific radioimmunoassays for PGF2 alpha, PGE2, and 6-keto-PGF1 alpha. Isolated glomeruli produced 1,740 pg x 10 min-1 x mg protein-1 of PGF2 alpha, 798 of 6-keto-PGF1 alpha, and 266 od PGE2. In prelabeled glomeruli angiotensin II causes a small but significant increase in 14C-labeled prostaglandins. Radioimmunoassay for 6-keto-PGF1 alpha showed that the angiotensin stimulation was specific for prostacyclin. Angiotensin II also affected the glomerular handling of [14C]arachidonate. It decreased the uptake of extracellular [14C]arachidonate and increased the incorporation of intracellular [14C]arachidonate into glomerular phospholipids. Based on these results, we propose that in the glomerulus angiotensin increases prostaglandin synthesis and stimulates deacylation and reacylation of phospholipids.

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