Pressor responses to vasopressin in rabbits with 3-day renal artery stenosis

1981 ◽  
Vol 240 (6) ◽  
pp. H862-H867 ◽  
Author(s):  
J. A. Johnson ◽  
S. Ichikawa ◽  
K. D. Kurz ◽  
W. L. Fowler ◽  
C. G. Payne
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Renal Artery ◽  
Renal Artery Stenosis ◽  
Peripheral Resistance ◽  
Plasma Renin ◽  
Cardiovascular Responses ◽  
Artery Stenosis ◽  
Vasopressin Infusion ◽  
Pressor Responses

One-kidney rabbits were subjected to renal artery stenosis, and acute experiments were performed 3 days later on conscious animals; one-kidney rabbits without renal artery stenosis served as controls. Rabbits with 3-day renal artery stenosis were normotensive and had normal values for plasma renin activity. Intravenous infusion of arginine vasopressin at 5 mU.min-1.kg body wt-1 for 5 min resulted in a significantly (P less than 0.01) greater increase in mean arterial pressure and total peripheral resistance (TPR) in the renal artery stenosis rabbits than in the controls. Infusion of the angiotensin II (AII) competitive antagonist, [Sar1, Ile8]AII, before the vasopressin infusion abolished the hyperresponsiveness to vasopressin in the renal artery stenosis rabbits and resulted in changes in mean arterial pressure and TPR that were approximately of the same magnitude as the controls. Infusion of [SAr1, Ile8]AII before vasopressin infusion in control rabbits did not alter the cardiovascular responses to vasopressin. Because previous studies have shown that 3-day renal artery stenosis rabbits have exaggerated pressor responses to norepinephrine and that this hyperresponsiveness to norepinephrine is blocked by [Sar1, Ile8]-AII, the present study with vasopressin provided evidence that the increased responsiveness in this model is not specific for a single pressor agent. These studies also demonstrated that AII plays an important role in mediating the exaggerated pressor responses to vasopressin in this prehypertensive model.

Fluid volumes and pressor responsiveness in two-kidney rabbits with renal artery stenosis

1982 ◽  
Vol 243 (5) ◽  
pp. H779-H787 ◽  
Author(s):  
J. A. Johnson ◽  
K. D. Kurz ◽  
S. Siripaisarnpipat ◽  
D. W. Zeigler ◽  
C. G. Payne
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Renal Artery ◽  
Renal Artery Stenosis ◽  
Body Fluid ◽  
Cardiovascular Responses ◽  
Artery Stenosis ◽  
Control Group ◽  
Ang Ii ◽  
Pressor Responses

This study examined body fluid volumes, the pressor responses to norepinephrine (NE), and the cardiovascular responses to NE before and during infusion of an angiotensin II (ANG II) antagonist in two-kidney rabbits with unilateral renal artery stenosis (RAS) of 3 and 30 day duration. Three separate experiments were performed. In the first experiment, plasma volume, extracellular fluid volume, and total body water were measured by the distribution volumes of radioiodinated serum albumin, 35SO4, and tritiated water, respectively. No differences were seen for any of these volumes between the 3- or 30-day RAS rabbits and their controls. In the second experiment, pressor responses to infusions of several doses of NE were examined; rabbits with 3- and 30-day RAS had exaggerated pressor responses to all doses of NE when compared with the control rabbits. In the third experiment, infusion of NE at 800 ng.min-1.kg body wt-1 resulted in more pronounced increases in mean arterial pressure and total peripheral resistance (TPR) in the 3- and 30-day RAS rabbits than in the controls; after infusion of [Sar1-Ile8] ANG II the increases in mean arterial pressure and TPR during NE infusion were blunted and were of the same magnitude as in the control group. In all experiments the 30-day RAS rabbits were hypertensive, whereas the 3-day RAS rabbits were normotensive; also, plasma renin activity (PRA) values were normal in both the 3- and 30-day RAS groups. These studies demonstrated that increases in body fluid volumes are not necessary for pressor and vascular hyperresponsiveness probably is mediated by ANG II, despite normal PRA values.

Adrenal gland in experimental renal hypertension.

1978 ◽  
Vol 234 (3) ◽  
pp. E267 ◽  
Author(s):  
A B Ribeiro ◽  
L R Krakoff
Keyword(s):  
Arterial Pressure ◽  
Renal Artery ◽  
Renal Artery Stenosis ◽  
Plasma Renin ◽  
Artery Stenosis ◽  
System Component ◽  
Independent Effect ◽  
Renin Substrate ◽  
Plasma Urea ◽  
High Salt Intake

The effect of total adrenalectomy on the mechanisms of arterial pressure control was studied in uninephrectomized rats with and without renal artery stenosis (Goldblatt one-kidney model). Four groups of rats were prepared and maintained on high-salt intake (1% NaCl): uninephrectomized-KI; KI + adrenalectomy-KIAx; uninephrectomized with renal artery stenosis-GI; and GI with adrenalectomy-GIAx. Over 3 wk blood pressure rose significantly in both GI and GIAx but the degree of increase in GI was greater. Hyponatremia, hyperkalemia, and increased plasma urea nitrogen were observed in both KIAx and GIAx. Plasma renin concentration (PRC) and plasma renine activity (PRA) were markedly increased and plasma renin substrate (PRS) was decreased in both adrenalectomized groups. Infusion of saralasin resulted in significant and similar reductions in mean arterial pressure (MAP) in KIAx and GIAx, but had no effect on MAP in KI and GI. These results allow approximations of the contribution to total MAP of identifiable components, which are: the total adrenal component, the renin-angiotensin system component, which partially compensates for loss of the adrenal secretions, and the independent effect of the renal artery clip. Thus, a multifactorial analysis of GI hypertension is provided.

scholarly journals Pressor responses to norepinephrine in rabbits with 3-day and 30-day renal artery stenosis. The role of angiotensin II.

1978 ◽  
Vol 43 (3) ◽  
pp. 437-446 ◽  
Author(s):  
S Ichikawa ◽  
J A Johnson ◽  
W L Fowler ◽  
C G Payne ◽  
K Kurz ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Renal Artery ◽  
Renal Artery Stenosis ◽  
Artery Stenosis ◽  
Pressor Responses

Plasma renin activity revealed renal artery stenosis concealed by aneurysms

Urology ◽  
2005 ◽  
Vol 65 (3) ◽  
pp. 592
Author(s):  
Masayuki Tanemoto ◽  
Takaaki Abe ◽  
Fumitoshi Satoh ◽  
Sadayoshi Ito
Keyword(s):  
Plasma Renin Activity ◽  
Renal Artery ◽  
Renal Artery Stenosis ◽  
Plasma Renin ◽  
Artery Stenosis ◽  
Renin Activity

AUTHOR'S REPLY

1985 ◽  
Vol 68 (4) ◽  
pp. 480-482 ◽  
Author(s):  
W. P. Anderson ◽  
P. I. Korner
Keyword(s):  
Arterial Pressure ◽  
Renal Artery ◽  
Renal Artery Stenosis ◽  
Artery Stenosis ◽  
Complete Occlusion ◽  
Baroreceptor Reflexes

Huisman and de Zeeuw consider that the acute haemodynamic events which follow renal artery stenosis may be due to spasm and subsequent relaxation of the renal artery, and disagree with our explanations [l, 21. In addition, they suggest that baroreceptor reflexes are responsible for the absence of a rise in arterial pressure after complete occlusion of the renal artery and reject our simple hydraulic explanation. We believe that these alternative explanations, though plausible, are incorrect.

Renal actions of angiotensin II in renovascular hypertension

1987 ◽  
Vol 65 (8) ◽  
pp. 1559-1565 ◽  
Author(s):  
W. P. Anderson ◽  
R. L. Woods ◽  
K. M. Denton ◽  
D. Alcorn
Keyword(s):  
Angiotensin Ii ◽  
Renal Artery ◽  
Glomerular Filtration ◽  
Renal Artery Stenosis ◽  
Renovascular Hypertension ◽  
Plasma Renin ◽  
Artery Stenosis ◽  
Filtration Fraction ◽  
Severe Stenosis ◽  
Glomerular Ultrafiltration

In renal artery stenosis severe enough to cause hypertension, angiotensin II maintains glomerular filtration rate (GFR) both in the initial high renin phase of hypertension and later when plasma levels are normal. Angiotensin II also maintains GFR in less severe stenosis, which does not cause hypertension. This homeostatic action of angiotensin II to maintain GFR has minimal effects on blood flow. In renal-wrap hypertension, plasma renin levels are elevated for longer than after renal artery stenosis, but in other respects this initial phase of the hypertension is similar to that after renal artery stenosis. GFR is reduced, the rate of development of hypertension is accelerated by angiotensin II, and angiotensin II maintains the glomerular filtration fraction. Renal resistance is markedly increased owing to both compression of the kidney by the hypertrophying renal capsule and to angiotensin II. Thus angiotensin II apparently plays a primarily homeostatic role in renovascular hypertension to maintain glomerular ultrafiltration. It is suggested that the angiotensin II may be formed intrarenally and may act on sites other than resistance blood vessels.

Effect of Percutaneous Transluminal Renal Angioplasty on Absolute Split Renal Function in Patients with Renovascular Hypertension. Influence of Age and Other Parameters

1993 ◽  
Vol 60 (1) ◽  
pp. 27-33
Author(s):  
M. Takeda ◽  
Y. Katayama ◽  
K. Saito ◽  
T. Tsutsui ◽  
T. Komeyama ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Renal Artery ◽  
Renal Artery Stenosis ◽  
Plasma Renin ◽  
Artery Stenosis ◽  
Renal Angioplasty ◽  
Split Renal Function ◽  
Percutaneous Transluminal Renal Angioplasty ◽  
Percutaneous Transluminal

Tc99m-dimercaptosuccinic acid renal uptake (DMSA uptake) was examined to assess the changes in split renal function following percutaneous transluminal renal angioplasty (PTRA) in 9 patients with a total of 12 renal artery stenoses and renovascular hypertension (RVH). The results were studied with respect to age, degree of renal artery stenosis, and renal vein renin ratio (RVRR) before PTRA. Although the degree of renal artery stenosis, systolic blood pressure, and peripheral blood plasma renin activity were improved 3 months after PTRA, neither the DMSA uptake of the affected kidneys nor that of the contralateral kidneys improved. Although restenosis occurred during the long follow-up period in one patient, DMSA uptake did not change in parallel with the degree of stenosis or RVRR. The degree of improvement in DMSA uptake, blood pressure, and plasma renin activity after PTRA in patients aged under 70 years was significantly higher than that in patients 70 years or older. Good improvement of renal function was attained in a 4-year-old boy, despite the fact that split renal function prior to PTRA was so poor that nephrectomy had been considered instead of PTRA. These results suggest that several factors before PTRA, such as DMSA uptake, degree of renal artery stenosis, and RVRR, are not absolutely predictive of results after PTRA, and that the effect of PTRA on blood pressure and renal function is greater in younger patients.

Hemodynamic effects of neurohypophyseal peptides with antidiuretic activity in dogs

1985 ◽  
Vol 249 (5) ◽  
pp. H1001-H1008 ◽  
Author(s):  
J. Schwartz ◽  
J. F. Liard ◽  
C. Ott ◽  
A. W. Cowley
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Peripheral Resistance ◽  
Cardiovascular Effects ◽  
Plasma Renin ◽  
Hemodynamic Effects ◽  
Antidiuretic Activity

Arginine vasopressin (AVP) is known to produce increases in total peripheral resistance (TPR) and mean arterial pressure (MAP) and decreases in heart rate (HR), cardiac output (CO), and plasma renin activity (PRA). Some recent observations with AVP and synthetic analogues have suggested that under certain conditions, AVP can induce cardiovascular and reninsecretory responses in the opposite directions. To characterize the receptors mediating these responses, the effects of AVP, oxytocin, and synthetic neurohypophyseal analogues with specific antidiuretic, vasoconstrictor, or oxytocic activities were studied in conscious dogs. AVP and 2-phenylalanine-8-ornithine-oxytocin (Phe2Orn8OT, a selective vasoconstrictor agonist) produced similar responses when infused at 10 ng X kg-1 X min-1. That is, TPR and MAP increased, and CO, HR, and PRA decreased. Pretreatment with a selective vasoconstrictor antagonist, [1-(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid) 2-(O-methyl)tyrosine]AVP, abbreviated d(CH2)5Tyr(Me)-AVP (10 micrograms/kg), blocked the actions of Phe2Orn8OT. However, in the presence of d(CH2)5Tyr(Me)AVP, AVP actually decreased TPR and increased CO, HR, and PRA. An analogue with selective antidiuretic activity, 4-valine-8-D-AVP (VDAVP, 10 ng X kg-1 X min-1), produced the same effects as the combination of vasopressin plus d(CH2)5Tyr(Me)AVP. Neither the effects of VDAVP nor of AVP plus antagonist were blocked by propranolol (1 mg/kg). These data indicate that vasopressin, by its antidiuretic activity, produces cardiovascular effects that are opposite to many of those produced by its vasoconstrictor action and that these effects are not dependent on mediation by beta-adrenoceptors.

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