Renal Denervation Prevents Sodium Retention and Hypertension in Salt-Sensitive Rabbits with Genetic Baroreflex Impairment

1996 ◽  
Vol 90 (4) ◽  
pp. 287-293 ◽  
Author(s):  
Marta Weinstock ◽  
Elena Gorodetsky ◽  
Ronald Kalman
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Renal Denervation ◽  
Plasma Renin ◽  
High Salt ◽  
Renin Activity ◽  
Group I ◽  
Group Ii

1. Rabbits with a genetic impairment in baroreflex control of heart rate become hypertensive on a high salt diet. The present study determined the effect of bilateral renal denervation on blood pressure and sodium balance after salt loading (four times normal intake; 28–36 mEq NaCl/day) in normotensive rabbits with high (Group I) and low (Group II) baroreflex sensitivity, respectively. 2. Eight rabbits in each group were denervated or sham-denervated 1 week before commencement of the high salt diet. Before operation, the two groups differed only in the gain of their cardiac baroreflex (Group I, −6.4 ± 0.4 beats min−1 mmHg−1; Group II, −3.2 ± 0.15 beats min−1 mmHg−1). 3. In Group I sham-denervated rabbits, mean arterial pressure remained unchanged, and plasma renin activity and heart rate fell significantly in response to the high salt. In Group II sham-denervated rabbits, mean arterial pressure increased by 10.6 ± 1.2 mmHg, and heart rate and plasma renin activity remained unchanged. Their cumulative Na+ retention and weight gain was more than twice that of Group I sham-denervated rabbits. 4. Renal denervation decreased plasma renin activity in both groups to <1 pmol Ang I h−1 ml−1, lowered cumulative Na+ retention from 102 ± 4 to 35 ± 5 mEq (P<0.01) and completely prevented the increase in mean arterial pressure in response to high salt in Group II. 5. The results suggest that Group II rabbits retain salt and fluid in response to their diet because of an abnormality in their control of renal nerve activity, possibly via vagal afferents. This results in blood pressure elevation because of an inability to lower peripheral resistance and heart rate in response to the increase in cardiac output. 6. Since they display several of the characteristics of salt-sensitive hypertensive humans, i.e. salt retention, normal plasma renin activity, but abnormal regulation of plasma renin activity and blood flow in response to salt loading, Group II are an appropriate model of human salt-induced hypertension.

Role of vasopressin in blood pressure regulation in conscious water-deprived dogs

1983 ◽  
Vol 244 (1) ◽  
pp. R74-R77 ◽  
Author(s):  
J. Schwartz ◽  
I. A. Reid
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Water Deprivation ◽  
Plasma Renin ◽  
Renin Activity ◽  
Pressure Regulation

The role of vasopressin in the regulation of blood pressure during water deprivation was assessed in conscious dogs with two antagonists of the vasoconstrictor activity of vasopressin. In water-replete dogs, vasopressin blockade caused no significant changes in mean arterial pressure, heart rate, plasma renin activity (PRA), or plasma corticosteroid concentration. In the same dogs following 48-h water deprivation, vasopressin blockade increased heart rate from 85 +/- 6 to 134 +/- 15 beats/min (P less than 0.0001), increased cardiac output from 2.0 +/- 0.1 to 3.1 +/- 0.1 1/min (P less than 0.005), and decreased total peripheral resistance from 46.6 +/- 3.1 to 26.9 +/- 3.1 U (P less than 0.001). Plasma renin activity increased from 12.4 +/- 2.2 to 25.9 +/- 3.4 ng ANG I X ml-1 X 3 h-1 (P less than 0.0001) and plasma corticosteroid concentration increased from 3.2 +/- 0.7 to 4.9 +/- 1.2 micrograms/dl (P less than 0.05). Mean arterial pressure did not change significantly. When the same dogs were again deprived of water and pretreated with the beta-adrenoceptor antagonist propranolol, the heart rate and PRA responses to the antagonists were attenuated and mean arterial pressure decreased from 103 +/- 2 to 91 +/- 3 mmHg (P less than 0.001). These data demonstrate that vasopressin plays an important role in blood pressure regulation during water deprivation in conscious dogs.

Factors that alter the plasma renin activity of the marmot

1983 ◽  
Vol 244 (6) ◽  
pp. R823-R831
Author(s):  
W. J. Ray ◽  
M. L. Zatzman
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Plasma Renin Activity ◽  
Peripheral Resistance ◽  
Plasma Renin ◽  
Renin Activity ◽  
Low Doses ◽  
Control Data ◽  
Volume Load

The effects of low doses of norepinephrine (NE) and furosemide and a volume load (nonhibernators only) on plasma renin activity (PRA), mean arterial pressure (MAP), heart rate (HR), left renal (RBF) and right iliac (IBF) blood flow, cardiac index (CI), and total peripheral resistance (TPR) were determined in euthermic and hibernating marmots. In nonhibernating marmots NE produced an increase in CI and TPR and a decrease in RBF. In hibernators this dose of NE caused an increase in MAP, HR, and renal resistance, whereas it decreased PRA and did not alter iliac resistance. Furosemide infusions led to an increase in PRA in both groups and an increase in TPR in nonhibernators. The volume load in nonhibernators produced only a decrease in PRA. A comparison of control data from the two groups indicated that the renal and iliac beds contribute only a small portion to the increase in TPR that occurs during hibernation.

Relationships between Plasma Renin Activity and Urinary and Plasma Catecholamines

1974 ◽  
Vol 48 (s2) ◽  
pp. 287s-290s ◽  
Author(s):  
U. Werner ◽  
H. Günnewig ◽  
K. D. Bock
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Renovascular Hypertension ◽  
Significant Positive Correlation ◽  
Plasma Renin ◽  
Primary Hypertension ◽  
Renin Activity ◽  
Positive Correlation ◽  
Noradrenaline Concentration

1. The relations between the changes in plasma renin activity (PRA) and urinary catecholamine excretion (UCA) or plasma noradrenaline concentration have been investigated (a) in patients with benign primary hypertension, with renovascular hypertension and with idiopathic asympatheticotonic hypotension (ASH), and (b) during orthostasis and after administration of frusemide, of the β-blocking agent tenormin, of clonidine and of dihydralazine. 2. In primary hypertension noradrenaline and mean arterial pressure (Pm) showed a close positive correlation. 3. The mean values of both PRA and UCA were higher in renovascular hypertension than in primary hypertension and extremely low in ASH. The overlap of individual values between the patient groups was markedly reduced by using the quotient PRA/UCA. There was a statistically significant positive correlation between PRA and UCA in primary hypertension and in renovascular hypertension, with a different slope of the regression lines. 4. The increase of PRA and of noradrenaline during orthostasis was closely correlated. Frusemide and β-receptor blockade changed the slope of the regression line by additional stimulation or inhibition respectively of PRA. 5. Clonidine decreased, and dihydralazine increased both PRA and noradrenaline concentration. These changes again showed a significant positive correlation. The fall of mean arterial pressure produced by clonidine was correlated with the decrease of PRA and of noradrenaline concentration.

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.

Protective effect of renal denervation on normotensive endotoxemia-induced acute renal failure in mice

2002 ◽  
Vol 283 (3) ◽  
pp. F583-F587 ◽  
Author(s):  
Wei Wang ◽  
Sandor A. Falk ◽  
Suparoek Jittikanont ◽  
Patricia E. Gengaro ◽  
Charles L. Edelstein ◽  
...  
Keyword(s):  
Renal Failure ◽  
Blood Flow ◽  
Acute Renal Failure ◽  
Glomerular Filtration Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Filtration Rate ◽  
Renal Denervation ◽  
Plasma Renin

Acute renal failure (ARF) contributes substantially to the high morbidity and mortality observed during endotoxemia. We hypothesized that selective blockade of the renal nerves would be protective against ARF during the early (16 h) stage of endotoxemia [5 mg lipopolysaccharide (LPS)/kg ip in mice]. At 16 h after LPS, there was no change in mean arterial pressure, but plasma epinephrine (4,604 ± 719 vs. 490 ± 152 pg/ml, P < 0.001), norepinephrine (2,176 ± 306 vs. 1,224 ± 218 pg/ml, P < 0.05), and plasma renin activity (40 ± 5 vs. 27 ± 2 ng · ml−1 · h−1, P < 0.05) were higher in the LPS-treated vs. control mice. The high plasma renin activity level decreased to the control level with renal denervation in endotoxemic mice. After intravenous injection of phentolamine (200 μg/kg), the decrement in mean arterial pressure was significantly greater in LPS-treated vs. control mice (19.4 ± 3.5 vs. 8.1 ± 1.5 mmHg, P < 0.01). Sixteen hours after LPS administration, there were significant decreases in glomerular filtration rate (52 ± 18 vs. 212 ± 23 μl/min, P < 0.01) and renal blood flow (0.58 ± 0.08 vs. 0.85 ± 0.06 ml/min, P < 0.01) in sham-operated mice. The decrement in glomerular filtration rate during endotoxemia was significantly attenuated in mice with denervated kidneys (32 vs. 79%). Moreover, there was no change in renal blood flow during endotoxemia in mice with renal denervation. The present results therefore demonstrate a protective role of renal denervation during normotensive endotoxemia-related ARF in mice, an effect that may be, at least in part, due to a diminished activation of the renin-angiotensin system.

scholarly journals Deoxycorticosterone Suppresses the Effects of Losartan in Nitric Oxide—Deficient Hypertensive Rats

2000 ◽  
Vol 11 (11) ◽  
pp. 1995-2000
Author(s):  
MARIA C. DE GRACIA ◽  
ANTONIO OSUNA ◽  
FRANCISCO O'VALLE ◽  
RAIMUNDO G. DEL MORAL ◽  
ROSEMARY WANGENSTEEN ◽  
...  
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Renal Injury ◽  
Renin Angiotensin System ◽  
Chronic Administration ◽  
Plasma Renin ◽  
Renin Activity ◽  
Ang Ii ◽  
Hypertensive Rats

Abstract. Chronic inhibition of the renin angiotensin system prevents increased BP and renal injury in NG-nitro-L-arginine methyl ester (L-NAME) hypertension. However, a relationship between plasma renin activity and the protective effect of chronic angiotensin II (Ang II) blockade has not been established. With this background, this study was undertaken to evaluate how the chronic administration of deoxycortisone acetate (DOCA) modifies the effects of losartan on BP, renal injury, and other variables in L-NAME hypertensive rats. The following groups were used: Control, DOCA, L-NAME, L-NAME + losartan, L-NAME + DOCA, and L-NAME + DOCA + losartan. Tail systolic BP was measured twice a week. After 4-wk evolution, mean arterial pressure and metabolic, morphologic, and renal variables were measured. The final mean arterial pressure values were 116 ± 6 mmHg for control, 107 ± 2 mmHg for DOCA, 151 ± 5 mmHg for L-NAME, 123 ± 2 mmHg for L-NAME + losartan, 170 ± 3 mmHg for L-NAME + DOCA, and 171 ± 5.5 mmHg for L-NAME + DOCA + losartan. Losartan prevented microalbuminuria, hyaline arteriopathy, and glomerulosclerosis of L-NAME hypertension but was ineffective in L-NAME + DOCA—treated rats. Plasma protein was significantly reduced in the L-NAME + DOCA group when compared with control and L-NAME groups, whereas no significant differences were observed in the other groups. Plasma renin activity was suppressed in the DOCA (0.55 ± 0.2) and L-NAME + DOCA (0.60 ± 10.2) groups but unsuppressed in the L-NAME + DOCA + losartan group (5.8 ± 1). The conclusion is that DOCA blocks the preventive effect of losartan on the increased BP and renal injury of L-NAME hypertension, which suggests that DOCA transforms L-NAME hypertension into an Ang II—independent model of hypertension. These data also suggest that losartan prevents L-NAME hypertension by blocking the activity of systemic Ang II.

Role of the vasoconstrictor and antidiuretic activities of vasopressin in inhibition of renin secretion in conscious dogs

1986 ◽  
Vol 250 (1) ◽  
pp. F92-F96 ◽  
Author(s):  
J. Schwartz ◽  
I. A. Reid
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Arginine Vasopressin ◽  
Plasma Renin ◽  
Renin Secretion ◽  
Conscious Dogs ◽  
Specific Antagonist

The nature of the activity of vasopressin that is responsible for the inhibition of renin secretion was studied in normally hydrated conscious dogs using intravenous infusions of vasopressin and analogues of vasopressin with selective antidiuretic and vasoconstrictor activity. Vasopressin (1.0 ng . kg-1 . min-1) increased mean arterial pressure (MAP) from 106 +/- 2 to 115 +/- 3 mmHg (P less than 0.05) and decreased heart rate (HR) from 81 +/- 6 to 56 +/- 5 beats/min (P less than 0.001). Plasma renin activity (PRA) decreased from 4.4 +/- 1.1 to 2.4 +/- 0.8 ng . ml-1 . 3 h-1 (P less than 0.05). A specific antagonist of the vasoconstrictor activity of vasopressin, d(CH2)5MeTyrAVP (10 micrograms/kg), completely blocked the cardiovascular and renin responses to vasopressin. A selective vasoconstrictor agonist, 2-phenylalanine-8-ornithine oxytocin (1.0 ng . kg-1 . min-1), increased MAP from 112 +/- 4 to 128 +/- 6 mmHg (P less than 0.001) and decreased HR from 69 +/- 3 to 47 +/- 4 beats/min (P less than 0.001). PRA decreased from 5.5 +/- 1.1 to 2.7 +/- 0.2 ng . ml-1 X 3 h-1 (P less than 0.001). In contrast, a selective antidiuretic agonist, 1-deamino-8-D-arginine vasopressin (1.0 ng . kg-1 . min-1) did not alter PRA, MAP, or HR. These results demonstrate that the acute inhibition of renin secretion by vasopressin in normally hydrated conscious dogs is due to vasoconstrictor rather than antidiuretic activity.

Effect of vasopressin blockade on blood pressure during water deprivation in intact and baroreceptor-denervated conscious dogs

1988 ◽  
Vol 254 (4) ◽  
pp. E490-E495 ◽  
Author(s):  
L. C. Gregory ◽  
E. W. Quillen ◽  
L. C. Keil ◽  
D. Chang ◽  
I. A. Reid
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Water Deprivation ◽  
Carotid Sinus ◽  
Plasma Renin ◽  
Renin Activity ◽  
Pressure Regulation ◽  
Marked Contrast

Previous studies have provided evidence that vasopressin plays an important role in blood pressure regulation during water deprivation. However, these investigations have been complicated by reflex compensatory increases in cardiac output and renin secretion. The aim of the present study was to investigate the effect of blockade of the vasoconstrictor action of vasopressin in conscious water-deprived dogs in which the low- and/or high-pressure baroreceptors were denervated to minimize reflex responses. Vasopressin blockade in sham-operated dogs (n = 7) did not change arterial pressure. Heart rate rose from 78 +/- 9 to 119 +/- 13 beats/min (P less than 0.01), and plasma renin activity increased from 10.9 +/- 2.1 to 21.6 +/- 4.6 ng.ml-1.3 h-1 (P less than 0.01). In carotid sinus-denervated dogs (n = 6), vasopressin blockade again failed to decrease arterial pressure. Heart rate increased from 105 +/- 10 to 132 +/- 10 beats/min (P less than 0.01), and plasma renin activity rose from 6.8 +/- 1.7 to 15.5 +/- 2.4 ng.ml-1.3 h-1 (P less than 0.01). The antagonist also failed to change blood pressure in cardiac-denervated dogs (n = 5). Heart rate increased from 111 +/- 9 to 119 +/- 1 beats/min (P less than 0.01), but plasma renin activity did not increase significantly. In marked contrast, vasopressin blockade in sinoaortic/cardiac-denervated dogs (n = 7) promptly decreased arterial pressure from 115 +/- 8 to 94 +/- 7 mmHg (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of renal denervation on plasma renin activity after aortic baroreceptor deafferentation

1991 ◽  
Vol 69 (8) ◽  
pp. 1237-1242 ◽  
Author(s):  
John Ciriello ◽  
James K. Simon ◽  
Paul F. Mercer
Keyword(s):  
Heart Rate ◽  
Plasma Renin Activity ◽  
Renal Denervation ◽  
Plasma Renin ◽  
Cardiovascular Regulation ◽  
The Other ◽  
Renin Activity ◽  
Renal Nerves ◽  
Neurogenic Hypertension ◽  
Aortic Depressor Nerve

Renal nerves are thought to play an important role in cardiovascular regulation under both normotensive and hypertensive conditions. In the present study the effect of renal denervation on the changes in plasma renin activity (PRA) after aortic baroreceptor deafferentation (tADN) were investigated in the rat. Bilateral renal denervation did not alter arterial pressure (AP, 100 ± 4 mmHg; 1 mmHg = 133.32 Pa), heart rate (HR, 363 ± 12 bpm), or PRA (2.9 ± 0.6 ng∙mL−1∙h−1) compared with the respective sham renal denervation values of 106 ± 3 mmHg (AP), 385 ± 13 bpm (HR), and 3.3 ± 0.7 ng∙mL−1∙h−1 (PRA). On the other hand, bilateral tADN resulted in significant increases in AP, HR, and PRA. One and 3 days after tADN, AP was 130 ± 4 and 127 ± 6 mmHg, HR was 461 ± 15 and 463 ± 20 bpm, and PRA was 9.1 ± 3.0 and 11.9 ± 4.5 ng∙mL−1∙h−1, respectively. Renal denervation before tADN prevented the increases in AP and PRA, but it did not affect the increase in HR. These data indicate that renal denervation does not alter basal PRA in normotensive animals but prevents the increased renin release observed in neurogenic hypertension. These data suggest that the increased PRA may be one of several factors that contributes to the elevated AP after tADN.Key words: aortic depressor nerve, afferent renal nerves, cardiovascular regulation, hypertension.

Postural Changes of Plasma Renin Activity after Renal Transplantation

1974 ◽  
Vol 48 (s2) ◽  
pp. 283s-286s
Author(s):  
A. Salvetti ◽  
F. Arzilli ◽  
P. Sassano ◽  
P. Gazzetti ◽  
P. Rindi
Keyword(s):  
Renal Transplantation ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Inverse Correlation ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Blocking Agent ◽  
Renin Activity ◽  
Postural Changes

1. Postural changes of plasma renin activity (PRA) before and after the administration of a beta-blocking agent (oxprenolol) were studied in nine patients with renal homotransplantation and in ten normal subjects. 2. In normal subjects PRA always increased during upright posture without any correlation with postural changes in mean arterial pressure. Oxprenolol reduced the postural increase of PRA. 3. A postural increase of PRA could be detected as early as 20–25 days after renal transplantation, and appeared with increasing frequency as time elapsed. 4. There was a significant inverse correlation (r−0.794,P <0.001) between the postural changes of PRA and those of mean arterial pressure. 5. These results suggest that in patients with renal homotransplantation the postural increase of PRA can only partly be due to circulating catecholamines or the sympathetic nervous system and may be explained by inverse changes in the mean arterial pressure.

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