Blood vessel-hormone interactions: angiotensin, bradykinin, and prostaglandins

1977 ◽  
Vol 232 (3) ◽  
pp. H305-H310 ◽  
Author(s):  
A. L. Blumberg ◽  
S. E. Denny ◽  
G. R. Marshall ◽  
P. Needleman
Keyword(s):  
Arachidonic Acid ◽  
Angiotensin Ii ◽  
Vascular Resistance ◽  
Initial Increase ◽  
Prostaglandin E ◽  
Induced Responses ◽  
Angiotensin I ◽  
Hormone Interactions ◽  
Pressor Responses ◽  
Mesenteric Vascular Resistance

Isolated Krebs-perfused rabbit-mesentery blood vessels release a prostaglandin E-like substance (PGE) when treated with angiotensin II, angiotensin I, arachidonic acid, or bradykinin. The specific competitive antagonist [Sar1,Ile8]angiotensin II, was found to inhibit angiotensin II-induced PGE release. The angiotensin antagonist did not block PGE release by bradykinin, whereas indomethacin blocked PGE release induced by all agonists. SQ-20881, the converting-enzyme and bradykininase inhibitor, decreased the PGE release by angiotensin I, enhanced the release by bradykinin, and did not affect release by angiotensin II. Pressor and depressor responses were obtained in mesenteric preparations constricted by epinephrine to a pressure of 60 mmHg. Angiotensin II induced an initial increase in mesenteric vascular resistance followed by a depressor response below basal pressure. The pressor responses were enhanced by indomethacin and the depressor responses were eliminated. Bolus injections of both bradykinin and arachidonic acid produced decreases in perfusion pressure, but indomethacin completely inhibited only the arachidonic acid-induced responses while only diminishing bradykinin-induced responses. The ability of angiotensin to increase mesenteric vascular resistance and to release PGE which decrease vascular resistance is discussed.

Effect of enalapril (MK-421), an orally active angiotensin I converting enzyme inhibitor, on blood pressure, active and inactive plasma renin, urinary prostaglandin E2, and kallikrein excretion in conscious rats

1984 ◽  
Vol 62 (1) ◽  
pp. 116-123 ◽  
Author(s):  
Ernesto L. Schiffrin ◽  
Jolanta Gutkowska ◽  
Gaétan Thibault ◽  
Jacques Genest
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Ace Inhibition ◽  
Renin Activity ◽  
Prostaglandin E ◽  
Converting Enzyme ◽  
Angiotensin I ◽  
Angiotensin I Converting Enzyme

The angiotensin I converting enzyme (ACE) inhibitor enalapril (MK-421), at a dose of 1 mg/kg or more by gavage twice daily, effectively inhibited the pressor response to angiotensin I for more than 12 h and less than 24 h. Plasma renin activity (PRA) did not change after 2 or 4 days of treatment at 1 mg/kg twice daily despite effective ACE inhibition, whereas it rose significantly at 10 mg/kg twice daily. Blood pressure fell significantly and heart rate increased in rats treated with 10 mg/kg of enalapril twice daily, a response which was abolished by concomitant angiotensin II infusion. However, infusion of angiotensin II did not prevent the rise in plasma renin. Enalapril treatment did not change urinary immunorcactive prostaglandin E2 (PGE2) excretion and indomethacin did not modify plasma renin activity of enalapril-treated rats. Propranolol significantly reduced the rise in plasma renin in rats receiving enalapril. None of these findings could be explained by changes in the ratio of active and inactive renin. Water diuresis, without natriuresis and with a decrease in potassium urinary excretion, occurred with the higher dose of enalapril. Enalapril did not potentiate the elevation of PRA in two-kidney one-clip Goldblatt hypertensive rats. In conclusion, enalapril produced renin secretion, which was in part β-adrenergically mediated. The negative short feedback loop of angiotensin II and prostaglandins did not appear to be involved. A vasodilator effect, apparently independent of ACE inhibition, was found in intact conscious sodium-replete rats.

scholarly journals PERAN KOMPLEKS JUKSTAGLOMERULUS TERHADAP RESISTENSI PEMBULUH DARAH

2013 ◽  
Vol 4 (3) ◽  
Author(s):  
Renny M. Toreh ◽  
Sonny J.R. Kalangi ◽  
Sunny Wangko
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Vascular Resistance ◽  
Sodium Intake ◽  
Angiotensin Receptor Blockers ◽  
Antihypertensive Agents ◽  
Angiotensin I ◽  
Renin Angiotensin ◽  
Renin Synthesis ◽  
Receptor Blockers

Abstract: As the main structural component of the renin-angiotensin-aldosterone system (RAAS), the juxtaglomerular complex plays a very important role in the regulation of vascular resistance. The synthesis and release of renin into the circulation occurs due to the decrease of blood pressure, loss of body fluid, and a decrease of sodium intake. Renin converts angiotensinogen into angiotensin I, which is further converted by the angiotensin converting enzyme (ACE) into angiotensin II. This angiotensin II causes vasoconstriction of blood vessels, resulting in an increase of vascular resistance and blood pressure. The ACE inhibitors and the angiotensin receptor blockers (ARBs) do not inhibit the RAAS completely since they cause an increase of renin activity. The renin blockers are more effective in inhibiting RAAS activity; therefore, these renin blockers can be applied as antihypertensive agents with fewer side effects. The RAAS activity can be inhibited by a decrease of renin synthesis in the juxtaglomerular complex by blocking the signals in the juxtaglomerular complex that stimulate renin synthesis, and by blocking the gap junctions in the juxtaglomerular complex. Keywords: juxtaglomerular complex, vascular resistance, RAAS.   Abstrak: Kompleks jukstaglomerulus sebagai komponen struktural utama sistem renin angiotensin berperan penting dalam pengaturan resistensi pembuluh darah. Sintesis dan pelepasan renin ke sirkulasi terjadi karena tekanan darah yang rendah, kehilangan cairan tubuh, dan kurangnya intake natrium. Renin akan memecah angiotensinogen menjadi angiotesin I yang kemudian secara cepat dikonversi oleh enzim pengonversi angiotensin  menjadi angiotensin II. Angiotensin II menyebabkan vasokontriksi pembuluh darah sehingga meningkatkan resistensi pembuluh darah yang pada akhirnya akan meningkatkan tekanan darah. ACEinhibitor dan ARB kurang sempurna dalam menghambat kerja SRAA oleh karena keduanya memutuskan rantai mekanisme timbal balik sehingga meningkatkan aktifitas renin. Penghambat renin lebih efektif digunakan untuk menghambat aktifitas SRAA sehingga penghambat renin dapat digunakan sebagai obat anti-hipertensi dan memiliki efek samping yang rendah. Metode penghambatan SRAA yang juga dapat dikembangkan ialah penghambatan sintesis renin dalam kompleks jukstaglomerulus dengan cara menekan sinyal-sinyal dalam kompleks jukstaglomerulus yang merangsang sintesis renin dan menghambat fungsi taut kedap yang terdapat dalam kompleks jukstaglomerulus. Kata kunci: kompleks juksta glomerulus, resistensi vaskular, SRAA.

scholarly journals Effects of Angiotensin I and Angiotensin II on Canine Hepatic Vascular Resistance

1973 ◽  
Vol 32 (1) ◽  
pp. 85-92 ◽  
Author(s):  
JOSEPH DI SALVO ◽  
STEVEN BRITTON ◽  
PATRICK GALVAS ◽  
THOMAS W. SANDERS
Keyword(s):  
Angiotensin Ii ◽  
Vascular Resistance ◽  
Angiotensin I

scholarly journals Role of Prostaglandins in Blood-Induced Vasoconstriction of Canine Cerebral Arteries

1988 ◽  
Vol 8 (1) ◽  
pp. 109-115 ◽  
Author(s):  
Sally A. Lang ◽  
Michael B. Maron
Keyword(s):  
Arachidonic Acid ◽  
Vascular Resistance ◽  
Topical Application ◽  
Cerebral Arteries ◽  
Cyclooxygenase Inhibitors ◽  
Prostaglandin E ◽  
Constant Flow ◽  
Thromboxane Synthetase ◽  
By Products

We tested the hypothesis that the vasoconstriction produced by the application of blood to the adventitial surfaces of the vessels of an isolated perfused canine circle of Willis preparation was mediated by products of prostaglandin metabolism. In this preparation (perfused at constant flow and outflow pressure), topical application of blood produced an average 16.6 ± 1.8 (SE) mm Hg increase in inflow pressure. This response could be prevented with four structurally dissimilar cyclooxygenase inhibitors (aspirin, indomethacin, ibuprofen, and meclofenamate), suggesting that the blood-induced increase in vascular resistance was mediated by prostaglandins. Imidazole, an inhibitor of thromboxane synthetase, had no effect on the blood response. Further support for the involvement of prostaglandins in this response was provided by additional experiments in which either arachidonic acid, prostaglandin E2 (PGE2), or PGF2α were administered. All three treatments produced vasoconstriction. These results suggest that the vessels of this preparation are capable of synthesizing vasoconstrictor prostaglandins and indicate that they are reactive to known vasoactive prostaglandins.

Effect of Sodium Depletion on the Steroidogenic and Pressor Actions of Angiotensin in the Rat

1979 ◽  
Vol 56 (4) ◽  
pp. 325-333 ◽  
Author(s):  
W. B. Campbell ◽  
J. M. Schmitz ◽  
H. D. Itskovitz
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Sodium Depletion ◽  
Angiotensin I ◽  
Arterial Blood ◽  
Serum Aldosterone ◽  
Pressor Responses ◽  
Angiotensin Iii

1. To investigate the relative roles of angiotensin II (AII) and des-Asp1-angiotensin II (angiotensin III) in the control of blood pressure and aldosterone release, the effects of seven angiotensin agonists on mean arterial blood pressure and serum aldosterone concentrations were compared in normal and sodium-depleted, conscious rats. 2. In normal rats, angiotensin I, α-Asp1-angiotensin II, β-Asp1-angiotensin II, and angiotensin II-amide were equipotent in elevating mean arterial blood pressure. Angiotensin III, des-Asp1-angiotensin I, and poly-O-acetylserine-angiotensin II were 25%, 25%, and 41% as potent as angiotensin II, respectively. After sodium depletion, pressor responses to these angiotensin peptides were reduced approximately 60–80% when compared with control responses. In contrast, pressor responses to noradrenaline were not significantly affected by sodium depletion. 3. Angiotensin II, β-Asp1-angiotensin II, angiotensin II-amide, and angiotensin III were equipotent in increasing serum aldosterone concentrations in normal animals. Angiotensin I was 59% and des-Asp1-angiotensin I only 5% as potent as angiotensin II in their abilities to release aldosterone. After sodium depletion, control serum aldosterone concentrations increased as did the slope of the dose—response curve for each angiotensin peptide. Angiotensin II was the most potent steroidogenic peptide in sodium-depleted rats with angiotensin III and β-Asp1-angiotensin II being 27%, angiotensin I 7%, angiotensin II-amide 3%, and des-Asp1-angiotensin I 1% as potent as angiotensin II in releasing aldosterone. Poly-O-acetylserine-angiotensin II has less steroidogenic effect than angiotensin II or III in both normal and sodium-depleted animals. 4. Infusions of the angiotensin II antagonist, Sar1-Ile8-angiotensin II, and the angiotensin III antagonist, Ile7-angiotensin III, enhanced aldosterone release in normal rats without altering blood pressure. After sodium depletion, Sar1-Ile8-angiotensin II decreased blood pressure without affecting aldosterone release whereas Ile7-angiotensin III diminished aldosterone release without altering blood pressure. 5. These data suggest that angiotensin II, independent of its conversion into angiotensin III, is an important regulator of steroidogenesis in the rat in normal sodium states. In sodium depletion, the octapeptide retains significant steroidogenic activity; however, the contribution of angiotensin III to its steroidogenic effects is increased.

Pulmonary vascular reactivity and hemodynamic changes in elastase-induced emphysema in hamsters

1992 ◽  
Vol 73 (4) ◽  
pp. 1474-1480 ◽  
Author(s):  
C. M. Tseng ◽  
S. Qian ◽  
W. Mitzner
Keyword(s):  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Right Ventricular ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Ventricular Hypertrophy ◽  
Vascular Reactivity ◽  
Pulmonary Arterial Pressure ◽  
Pressor Responses ◽  
Pulmonary Arterial

Changes in pulmonary hemodynamics and vascular reactivity in emphysematous hamsters were studied in an isolated lung preparation perfused at constant flow with blood and 3% dextran. Hamsters were treated with intratracheal porcine pancreatic elastase at 70 days of age, and experimental studies were conducted at 1, 3, and 8 mo after treatment. Baseline pulmonary arterial pressure in elastase-treated lungs was increased compared with saline-treated control lungs 1 mo after treatment, but this increase did not progress at 3 and 8 mo. Increases in pulmonary arterial pressure in elastase-treated lungs were temporally correlated with the morphological development of emphysema and right ventricular hypertrophy; both of these were evident at 1 mo after treatment and showed little change thereafter. Pressor responses to hypoxia and angiotensin II were not different between elastase-treated and control lungs at 1 and 3 mo. At 8 mo, however, pressor responses in emphysematous lungs to 0% O2 (but not to angiotensin II) were significantly increased. This was the result of a lack of the normal age-related fall in the hypoxic pressor response. Our results suggest that the right ventricular hypertrophy found in these emphysematous animals results from a chronically increased pulmonary vascular resistance. Furthermore, increases in pulmonary vascular resistance in the early development of emphysema are likely a result of the loss of vascular beds and supporting connective tissue.

Cardiovascular effects of posterior hypothalamic stimulation in baroreflex-denervated rats

1990 ◽  
Vol 259 (3) ◽  
pp. H720-H727 ◽  
Author(s):  
K. W. Barron ◽  
C. M. Heesch
Keyword(s):  
Electrical Stimulation ◽  
Vascular Resistance ◽  
Cardiovascular Effects ◽  
Posterior Hypothalamus ◽  
Intact Group ◽  
Pressor Responses ◽  
The Central Nervous System ◽  
Mesenteric Vascular Resistance ◽  
Posterior Hypothalamic Stimulation ◽  
Stimulation Of

The overall purpose of this study was to examine the effect of sinoaortic baroreceptor denervation (SAD) on the cardiovascular and sympathetic outflow responses to electrical stimulation of the posterior hypothalamus. In anesthetized rats that had undergone SAD 7-10 days before experimentation, electrical stimulation of the posterior hypothalamus elicited greater increases in mean arterial pressure, iliac vascular resistance, mesenteric vascular resistance, and lumbar sympathetic nerve activity than in sham-operated baroreceptor-intact animals. Similarly, the pressor effects of intravenous norepinephrine were also augmented in the baroreceptor-denervated group compared with the baroreceptor-intact group. When posterior hypothalamic and intravenous norepinephrine pressor stimuli, which produced equivalent pressor responses in sham-operated baroreceptor-intact animals, were compared in baroreceptor-denervated animals, the pressor effects of the central hypothalamic stimulus were enhanced to a greater degree than the norepinephrine pressor effects. These data provide evidence that arterial baroreceptor reflexes exert greater buffering of pressor stimuli initiated from the central nervous system compared with pressor responses due to peripheral vascular vasoconstrictor agents.

Intrarenal Formation of Angiotensin II in the Rat: Interference by Saralasin and SQ 20881

1974 ◽  
Vol 48 (s2) ◽  
pp. 37s-40s
Author(s):  
H. Zschiedrich ◽  
K. G. Hofbauer ◽  
E. Hackenthal ◽  
G. D. Baron ◽  
F. Gross
Keyword(s):  
Angiotensin Ii ◽  
Vascular Resistance ◽  
Plasma Renin ◽  
Rat Plasma ◽  
Renal Vascular Resistance ◽  
Angiotensin I ◽  
Renin Substrate ◽  
Vasoconstrictor Effect ◽  
Renal Vascular ◽  
Dose Dependent

1. Isolated rat kidneys were perfused with a medium free of components of the renin-angiotensin system. 2. Angiotensin II, angiotensin I, tetradecapeptide renin substrate or rat plasma renin substrate added to the medium caused a dose-dependent increase of renal vascular resistance. 3. The vasoconstrictor effect of angiotensin II was inhibited by 1-Sar-8-Ala-angiotensin II (Saralasin). The inhibition was dose-dependent, being complete at the highest doses applied. In this dose range, Saralasin increased renal vascular resistance. Saralasin also inhibited vasoconstriction induced by tetradecapeptide renin substrate. 4. The vasoconstrictor effect of angiotensin I was suppressed by SQ 20881, up to a maximum of 87% depending on the dose. Similarly the increase in renal vascular resistance induced by a purified preparation of rat plasma renin substrate was inhibited by 55%; no effect on the action of tetradecapeptide renin substrate was observed. 5. The data suggest that, within the kidney, angiotensin I is converted into angiotensin II to the extent of about 1.25%. Since no angiotensin I is formed from synthetic renin substrate, the vasoconstrictor effect of the tetradecapeptide may be either due to a direct interaction with the angiotensin II receptor or the consequence of the intrarenal formation of angiotensin II. In contrast, the results with rat plasma renin substrate suggest that angiotensin I is formed from ‘natural’ substrate and is subsequently converted into angiotensin II.

Pressor Response to Angiotensin I and Angiotensin II: The Site of Conversion of Angiotensin I

1972 ◽  
Vol 43 (6) ◽  
pp. 839-849 ◽  
Author(s):  
E. C. Osborn ◽  
G. Tildesley ◽  
P. T. Pickens
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Pressor Response ◽  
Left Ventricular ◽  
Angiotensin I ◽  
Intravenous Injections ◽  
Pressor Responses ◽  
The Difference

1. The pressor responses to angiotensin I were compared with those to angiotensin II after injections into the left ventricle and jugular vein in the sheep, dog and pig. 2. The ability of angiotensin I to raise the blood pressure was less than that of angiotensin II with both routes of injection, a difference which was more marked after ventricular injection. 3. When equipressor doses of the hormones were given there was a delay of 1–3 s in the onset of the pressor response to angiotensin I compared with angiotensin II after left-ventricular injections; the difference in the delay in onset was less apparent with intravenous injections. 4. The development of the pressor responses was similar with both hormones when equipressor doses were used but the rises in blood pressure were more prolonged with angiotensin I, especially when given by the left-ventricular route. 5. The in vitro rate of activation of angiotensin I by blood was much slower than the apparent in vivo formation of angiotensin II.

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