Removal of angiotensins from the systemic circulation

1968 ◽  
Vol 46 (2) ◽  
pp. 175-178 ◽  
Author(s):  
Pierre Biron ◽  
Philippe Meyer ◽  
Jean-Claude Panisset
Keyword(s):  
Pulmonary Circulation ◽  
Systemic Circulation ◽  
The Other ◽  
Main Process ◽  
Extraction Percentage ◽  
Pressor Responses ◽  
Anesthetized Dogs ◽  
Vascular Beds ◽  
Renal Vascular

The extraction of α-angiotensin and its aminopeptidase-resiistant analogue β-angiotensin by the pulmonary, hepatoportal, femoral, and renal vascular beds was studied in normal anesthetized dogs and rats by comparing the systemic pressor responses to infusions into the afferent and efferent vessel of each organ. The extraction percentage of both peptides by the pulmonary circulation was negligible whereas it averaged 70% for α-angiotensin and 63% for the β-analogue in the other three systemic vascular beds studied. It is concluded that the main process responsible for the clearing of angiotensin from the systemic circulation is not the activity of circulating angiotensinases but rather occurs in the tissues.

Muscle metaboreflex control of cardiac output and peripheral vasoconstriction exhibit different latencies

2000 ◽  
Vol 278 (2) ◽  
pp. H530-H537 ◽  
Author(s):  
Robert A. Augustyniak ◽  
Eric J. Ansorge ◽  
Donal S. O'Leary
Keyword(s):  
Cardiac Output ◽  
Vascular Occlusion ◽  
Systemic Arterial Pressure ◽  
Vascular Conductance ◽  
Muscle Metaboreflex ◽  
Peripheral Vasoconstriction ◽  
Pressor Responses ◽  
Vascular Beds ◽  
The Individual ◽  
Renal Vascular

Experiments were designed to determine 1) the mechanisms mediating metaboreflex-induced increases in systemic arterial pressure (SAP) in response to total vascular occlusion of hindlimb blood flow [e.g., increases in cardiac output (CO) vs. peripheral vasoconstriction] and 2) whether the individual mechanisms display differential latencies for the onset of the responses. Responses were observed in seven dogs performing steady-state treadmill exercise of mild and moderate workloads (3.2 km/h at 0% grade and 6.4 km/h at 10% grade). Differential latencies were exhibited among CO, nonischemic vascular conductance (NIVC; conductance to all nonischemic vascular beds), and renal vascular conductance (RVC), with peripheral vasoconstriction significantly preceding metaboreflex-mediated increases in CO. In addition, the latencies for SAP were not different from those for NIVC or RVC at either workload. During the lower workload there were small increases and then subsequent decreases in CO before the metaboreflex-induced increase in CO, which did contribute somewhat to the initial increases in SAP. However, the increases in CO mediated by the metaboreflex occurred significantly later than the initial increases in SAP. Therefore, we conclude that the substantial metaboreflex-mediated pressor responses that occur during the initial phase of total vascular occlusion during mild and moderate exercise are primarily caused by peripheral vasoconstriction.

Disappearance of Angiotensin II and Noradrenaline from the Renal and Femoral Circulations of the Dog

1980 ◽  
Vol 58 (1) ◽  
pp. 29-35 ◽  
Author(s):  
M. J. S. Miller ◽  
G. C. Scroop
Keyword(s):  
Angiotensin Ii ◽  
Renal Artery ◽  
Femoral Artery ◽  
Pressor Response ◽  
Intravenous Route ◽  
Vascular Bed ◽  
Pressor Responses ◽  
Vascular Beds ◽  
Degree Of Extraction ◽  
Renal Vascular

1. The relative ability of the renal and femoral vascular beds to remove infused angiotensin II and noradrenaline was examined in anaesthetized greyhounds. 2. The degree of extraction of infused drug by each vascular bed was expressed as a percentage, calculated by comparing the pressor response to intra-arterial infusion with that obtained when the same dose was administered by the intravenous route. 3. When compared with the same dose given intravenously, the pressor responses after renal artery administration of angiotensin II were reduced by a mean of 77·8 ± 4·1% (mean ± sem, n = 12), whereas those after femoral artery infusions at the same dose were reduced by a mean of only 27·2 ± 4·9%(n = 12). 4. The pattern of extraction seen with noradrenaline infusions administered in a similar manner was the reverse of that with angiotensin II. There was a 28·9 ± 6·8% (n = 7) reduction in pressor responses to renal artery infusions; in contrast, femoral artery infusions of the same dose exhibited a 99·0 ± 1·0% (n = 7) reduction in the pressor responses. 5. Local arterial administration of the angiotensin II competitive antagonist, [Sar1,Ile8]angiotensin II, potentiated the systemic pressor responses to renal artery infusions of angiotensin II, but not those to femoral artery infusions. 6. It is suggested that the marked ability of the renal vascular bed to remove circulating angiotensin II may, in part, involve receptor-binding, although this seems not to be the case in the femoral vascular bed.

EXTRAHEPATIC AND EXTRARENAL RENIN INACTIVATION IN THE DOG

1974 ◽  
Vol 60 (2) ◽  
pp. 217-222
Author(s):  
R. FAGARD ◽  
E. FOSSION ◽  
M. CAMPFORTS ◽  
A. AMERY
Keyword(s):  
Blood Vessels ◽  
Pulmonary Circulation ◽  
Plasma Renin ◽  
Glass Container ◽  
Plasma Renin Concentration ◽  
Vascular Beds ◽  
Extrarenal Renin

SUMMARY It was demonstrated previously that renin disappears quickly from the circulation after nephrectomy in the hepatectomized dog. In the present study the plasma renin concentration (PRC) was measured in the efferent and afferent blood vessels of several vascular beds (pulmonary circulation, splanchnic region, spleen, both inferior limbs and pelvis, head) in the anhepatic and in the anhepatic and anephric dog in order to investigate extrarenal and extrahepatic renin inactivation. However, no significant arteriovenous differences in PRC could be traced. The blood of these dogs kept in vitro at 37 °C in a glass container showed no decline in PRC within 3 h of removal. Therefore no specific extrahepatic and extrarenal renin-inactivating mechanism was found which could explain the rapid disappearance of renin from the blood in vivo in the anhepatic and anephric dog.

Endothelium-derived relaxing factor in regulation of basal cardiopulmonary and renal function

1991 ◽  
Vol 261 (2) ◽  
pp. R323-R328 ◽  
Author(s):  
M. A. Perrella ◽  
F. L. Hildebrand ◽  
K. B. Margulies ◽  
J. C. Burnett
Keyword(s):  
Renal Function ◽  
Competitive Inhibitor ◽  
Vehicle Group ◽  
Relaxing Factor ◽  
Anesthetized Dogs ◽  
Endothelium Derived Relaxing Factor ◽  
Renal Vascular ◽  
Renal Responses

The endothelium has emerged as an important modulator of vascular tone by producing both vasodilating and vasoconstricting substances. In vitro studies have demonstrated that endothelial cells produce endothelium-derived relaxing factor (EDRF), which promotes vasodilation via the stimulation of intracellular guanosine 3',5'-cyclic monophosphate (cGMP). However, the role of EDRF in the basal regulation of cardiopulmonary and renal function is not well defined. The present study was therefore designed to assess the function of EDRF by studying two groups of normal anesthetized dogs, of which one received a competitive inhibitor to EDRF generation, NG-monomethyl-L-arginine (L-NMMA; 50 micrograms.kg-1.min-1 iv), and the other received a vehicle. The L-NMMA infusion produced no significant increase in mean arterial pressure but marked increases in systemic, pulmonary, and renal vascular resistances compared with the vehicle group. Although renal blood flow decreased with L-NMMA, no changes were observed in glomerular filtration rate or sodium excretion. Associated with the cardiopulmonary and renal responses with L-NMMA was a modest increase in plasma endothelin (7.9 +/- 1.3 to 10.2 +/- 1.8 pg/ml, P less than 0.05), an endothelium-derived vasoconstrictor. No alteration was observed in plasma or urinary cGMP with EDRF inhibition. These cardiopulmonary and renal responses with L-NMMA may be attributed not only to EDRF inhibition but to an imbalance between endothelium-derived relaxing and contracting factors.

Effects of exercise training on the vascular reactivity of the whole kidney circulation in rabbits

2004 ◽  
Vol 97 (2) ◽  
pp. 683-688 ◽  
Author(s):  
Roger De Moraes ◽  
Giovanni Gioseffi ◽  
Antonio C. L. Nóbrega ◽  
Eduardo Tibiriçá
Keyword(s):  
Exercise Training ◽  
Vascular Reactivity ◽  
Perfusion Pressure ◽  
Rabbit Kidney ◽  
Constant Flow ◽  
Renal Circulation ◽  
New Zealand White Rabbits ◽  
Vascular Beds ◽  
Renal Vascular ◽  
Isolated Kidneys

Exercise training is known to improve vasodilating mechanisms mediated by endothelium-dependent relaxing factors in the cardiac and skeletal muscle vascular beds. However, the effects of exercise training on visceral vascular reactivity, including the renal circulation, are still unclear. We used the experimental model of the isolated perfused rabbit kidney, which involves both the renal macro- and microcirculation, to test the hypothesis that exercise training improves vasodilator mechanisms in the entire renal circulation. New Zealand White rabbits were pen confined (Sed; n = 24) or treadmill trained (0% grade) for 5 days/wk at a speed of 18 m/min during 60 min over a 12-wk period (ExT; n = 24). Kidneys isolated from Sed and ExT rabbits were continuously perfused in a nonrecirculating system under conditions of constant flow and precontracted with norepinephrine (NE). We assessed the effects of exercise training on renal vascular reactivity using endothelial-dependent [acetylcholine (ACh) and bradykinin (BK)] and -independent [sodium nitroprusside (SNP)] vasodilators. ACh induced marked and dose-related vasodilator responses in kidneys from Sed rabbits, the reduction in perfusion pressure reaching 41 ± 8% ( n = 6; P < 0.05). In the kidneys from ExT rabbits, vasodilation induced by ACh was significantly enhanced to 54 ± 6% ( n = 6; P < 0.05). In contrast, BK-induced renal vasodilation was not enhanced by training [19 ± 8 and 13 ± 4% reduction in perfusion pressure for Sed and ExT rabbits, respectively ( n = 6; P > 0.05)]. Continuous perfusion of isolated kidneys from ExT animals with Nω-nitro-l-arginine methyl ester (l-NAME; 300 μM), an inhibitor of nitric oxide (NO) biosynthesis, completely blunted the additional vasodilation elicited by ACh [reduction in perfusion pressure of 54 ± 6 and 38 ± 5% for ExT and l-NAME + ExT, respectively ( n = 6; P < 0.05)]. On the other hand, l-NAME infusion did not affect ACh-induced vasodilation in Sed animals. Exercise training also increased renal vasodilation induced by SNP [36 ± 7 and 45 ± 10% reduction in perfusion pressure for Sed and ExT rabbits, respectively ( n = 6; P < 0.05)]. It is concluded that exercise training alters the rabbit kidney vascular reactivity, enhancing endothelium-dependent and -independent renal vasodilation. This effect seems to be related not only to an increased bioavailability of NO but also to the enhanced responsiveness of the renal vascular smooth muscle to NO.

scholarly journals Pathogenesis of Arterial Lesions Induced by Dopaminergic Compounds in the Rat

1989 ◽  
Vol 17 (1_part_2) ◽  
pp. 203-213 ◽  
Author(s):  
William D. Kerns ◽  
Emanuel Arena ◽  
Richard A. Macia ◽  
Peter J. Bugelski ◽  
William D. Matthews ◽  
...  
Keyword(s):  
Arterial Injury ◽  
Mesenteric Arteries ◽  
Receptor Subtypes ◽  
Alpha Adrenoceptors ◽  
Beta Adrenoceptor ◽  
Alpha Adrenoceptor ◽  
Alpha Adrenoceptor Agonists ◽  
Arterial Lesions ◽  
Vascular Beds ◽  
Renal Vascular

Fenoldopam mesylate (FM), a selective post-junctional dopaminergic (DA1) vasodilator, causes lesions of large caliber splanchnic arteries (100–800 μm) in the rat characterized by necrosis of medial smooth muscle cells and hemorrhage. FM does not induce lesions in other vascular beds of the rat, or in dogs or monkeys. Dopamine, like FM, causes hemorrhagic lesions of large caliber splanchnic arteries in the rat, as well as fibrinoid necrosis of small caliber arteries (<100 μm) of the splanchnic, cerebral, coronary and renal vascular beds. Dopamine is an alpha- and beta-adrenoceptor and a dopaminergic receptor agonist. Because these arterial lesions are thought to result from the pharmacologic activity of these 2 compounds, we sought to ascertain the presence of DA1 receptors in mesenteric arteries of the rat and to determine the role of these or other vascular receptor subtypes in lesion induction. We also studied the process of repair after arterial injury caused by FM or dopamine. The presence of DA1 receptors was confirmed in isolated perfused mesenteric arteries by standard pharmacologic techniques; stimulation by FM resulted in vasodilation which was inhibited by the DA1 receptor antagonist SK&F 83566-C. Likewise, SK&F 83566-C prevented the induction of hemorrhagic lesions of large caliber arteries in rats upon infusion of FM or dopamine. In rats co-exposed to the alpha-adrenoreceptor antagonist phenoxybenzamine (PBZ) and either FM or dopamine, the incidence and severity of hemorrhagic lesions of large caliber arteries were increased, but PBZ prevented the formation of dopamine-induced fibrinoid lesions in arteries of small caliber. Rats exposed concurrently to dopamine, phenoxybenzamine, and SK&F 83566-C were free of all arterial lesions. Thus, the induction of splanchnic arterial lesions in the rat by dopamine and FM is caused by stimulation of, and interaction between, alpha-adrenoceptors and dopaminergic DA1 receptors. Fibrinoid lesions of small arteries (alpha-adrenoceptor-mediated) were repaired, as observed morphologically by 14 d after exposure to dopamine. Hemorrhagic lesions of large caliber arteries (DA1 receptor-mediated) had undergone significant repair by 28 d after exposure to FM but these arteries possessed a thicker media surrounded by adventitial fibrosis. Thus, morphologically distinct receptor-mediated splanchnic arterial lesions induced by dopaminergic and alpha-adrenoceptor agonists follow a markedly different course of repair. Arterial lesions induced by FM or dopamine by activation of post-junctional dopaminergic DA1 receptors may represent a model of polyarteritis nodosa.

Ventricular fibrillation during uniform myocardial anoxia due to asphyxia

1960 ◽  
Vol 198 (5) ◽  
pp. 955-958 ◽  
Author(s):  
Jay D. Coffman ◽  
D. E. Gregg
Keyword(s):  
Cardiac Arrest ◽  
Ventricular Fibrillation ◽  
Potassium Level ◽  
Serum Potassium Level ◽  
Current Theory ◽  
The Other ◽  
Right Atrial ◽  
Serum Electrolytes ◽  
Anesthetized Dogs ◽  
A Current

Thirty-three anesthetized dogs of varying weights were subjected to complete asphyxia by tracheal occlusion to produce uniform anoxia of the heart. Eleven showed electrocardiographic evidence of ventricular fibrillation while the other twenty-two demonstrated cardiac arrest. The development of ventricular fibrillation correlated with the heavier body and heart weights and with a lower average right atrial serum potassium level as compared to the dogs not fibrillating. Other serum electrolytes, pH, body temperature and sex showed no correlation with the arrhythmia. The importance of the fact that large dogs have a greater susceptibility to develop ventricular fibrillation during uniform anoxia of the heart is discussed in relation to experimental research on dogs and to a current theory of the cause of ventricular fibrillation.

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