Renal autoregulation in chronically catheterized conscious rats

1984 ◽  
Vol 247 (2) ◽  
pp. F229-F233 ◽  
Author(s):  
K. P. Conrad ◽  
T. Brinck-Johnsen ◽  
M. Gellai ◽  
H. Valtin
Keyword(s):  
Arterial Pressure ◽  
Renal Plasma Flow ◽  
Transient State ◽  
Plasma Renin ◽  
Conscious Rat ◽  
Absolute Level ◽  
Absolute Value ◽  
Conscious Rats ◽  
Control Value ◽  
Aortic Cuff

We examined renal hemodynamics and arterial plasma renin activity (PRA) concurrently in trained chronically catheterized conscious rats during decreased and elevated renal arterial pressure (RAP). Control RAP had an absolute value of 112 +/- 2 mmHg (mean +/- SE). During inflation of a suprarenal aortic cuff, glomerular filtration rate (GFR) and effective renal plasma flow (ERPF) were autoregulated down to 82% of control RAP. Within this range GFR averaged 107 +/- 5% and ERPF 114 +/- 10% of the control value. During inflation of the infrarenal aortic cuff, RAP increased by 24 +/- 2% to an absolute level of 139 +/- 5 mmHg; this elevation was associated with autoregulation of both GFR (100 +/- 5% of control) and ERPF (94 +/- 6% of control). Arterial PRA had an absolute value during control conditions of 2.1 +/- 0.2 ng ANG I X ml-1 X h-1. It was not significantly altered within the autoregulatory range, being 104 +/- 10% of control during lowered RAP and 120 +/- 15% of control during elevated RAP. Nor, in separate experiments, was PRA changed significantly during the transient state, i.e., at 5, 10, or 30 min after RAP was lowered to an autoregulatory level. These studies demonstrate that, in the conscious rat, there is considerable autoregulatory capacity both below and above resting arterial pressure, and that GFR and ERPF are autoregulated concomitantly. Arterial PRA was not altered significantly within the autoregulatory range.

Acute and chronic actions of bradykinin on renal function and arterial pressure

1985 ◽  
Vol 248 (1) ◽  
pp. F87-F92 ◽  
Author(s):  
J. P. Granger ◽  
J. E. Hall
Keyword(s):  
Arterial Pressure ◽  
Renal Plasma Flow ◽  
Urine Volume ◽  
Plasma Renin ◽  
Urinary Sodium Excretion ◽  
Renal Perfusion ◽  
Acute Effects ◽  
Plasma Aldosterone Concentration ◽  
Control Value ◽  
Renal Vascular

The present study was designed to examine the acute and chronic effects of increased levels of circulating bradykinin (BK) on control of renal hemodynamics, electrolyte excretion, and arterial pressure. Intrarenal infusion of BK (50 ng X kg-1 X min-1) for 60 min in five anesthetized dogs with renal perfusion pressure maintained at a constant level of 108 +/- 1 mmHg had no significant effect on glomerular filtration rate (GFR), whereas it increased renal blood flow (RBF) from a control value of 230 +/- 14 to 282 +/- 18, 266 +/- 15, and 253 +/- 17 ml/min after 15, 30, and 60 min of infusion, respectively. Acute intrarenal infusion of BK also increased urine volume (UV) from 0.255 +/- 0.044 to 0.523 +/- 0.103 ml/min and urinary sodium excretion (UNaV) from 5.72 +/- 1.5 to 13.7 +/- 3.4 mueq/min. To determine whether the potent acute effects of BK on RBF, UV, and UNaV lead to a chronic reduction in arterial pressure, BK (50 ng X kg-1 X min-1) was infused intrarenally for 7 days in conscious dogs. Intrarenal infusion of BK for 7 days had no significant effect on GFR, UNaV, UV, or arterial pressure. However, BK elevated renal plasma flow and decreased renal vascular resistance throughout the 7 days of infusion. Chronic intrarenal BK infusion caused no significant changes in plasma renin activity or plasma aldosterone concentration. Results from these studies indicate that although increased levels of bradykinin in the renal circulation can have potent acute effects on RBF, UV, and UNaV, these effects on UV and UNaV are not sustained and therefore do not result in long-term changes in arterial pressure.

Effect of Narcotic Agents and of Bleeding on Systemic and Renal Haemodynamics in Healthy and CCl4-treated Cirrhotic Rats

1997 ◽  
Vol 93 (6) ◽  
pp. 549-556 ◽  
Author(s):  
G. Van Roey ◽  
P. Lijnen ◽  
R. Verbesselt ◽  
A. Verbruggen ◽  
J. Fevery
Keyword(s):  
Arterial Pressure ◽  
Plasma Volume ◽  
Renal Plasma Flow ◽  
Portal Pressure ◽  
Plasma Renin ◽  
Repeated Measurements ◽  
Peripheral Vasodilatation ◽  
Profound Hypotension ◽  
Awake Rat ◽  
Related Mortality

1. The haemodynamic effects of different narcotic agents have been tested in healthy rats and in rats with cirrhosis. 2. Pentobarbital suppresses the sympathetic nervous system. Susceptibility to ketamine is unpredictable, leading to both insufficient pain relief and narcosis related mortality. The combination diazepam—fluanisone induces profound hypotension. After insertion of catheters, awake, freely moving rats are stable and not distressed. This allows repeated measurements after manipulation. Moreover, procedure-related mortality is low and rats have a better stress response. 3. In the awake animal, arterial pressure is 126 ± 10 for healthy animals, and 111 ± 16 and 102 ± 10 mmHg for cirrhotic animals without and with ascites, respectively (P = 0.018). The respective values for portal pressure are 6.9 ± 1.4, 11.6 ± 2.5 and 16.2 ± 2.9 mmHg (P = 0.0001). After a bleeding, arterial pressure is better preserved than portal pressure in the three groups (P < 0.0001). Plasma volume in cirrhotic rats exceeds that of healthy rats. Plasma renin activity, aldosterone and catecholamines do not differ between the groups studied. In cirrhotic rats with and without ascites, glomerular filtration rate tends to be higher (P = 0.12), renal plasma flow is elevated (P = 0.001) and nitration fraction is lower (P = 0.002) than in healthy rats. 4. In conclusion, haemodynamic experiments in the cirrhotic rat should be performed in the awake rat. Arterial hypotension, impaired filtration fraction, enlarged plasma volume and portal hypertension are present in cirrhosis before the development of ascites. This can as well be explained by splanchnic pooling of blood, as by peripheral vasodilatation. The decrease in portal pressure with preserved arterial pressure after a bleeding protects cirrhotic rats from ongoing variceal bleeding.

Hypertension Induced by Prolonged Intracoronary Administration of Dobutamine in Conscious Dogs

1978 ◽  
Vol 54 (2) ◽  
pp. 153-160 ◽  
Author(s):  
J.-F. Liard
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Peripheral Resistance ◽  
Extracellular Fluid ◽  
Electromagnetic Flowmeter ◽  
Plasma Renin ◽  
Conscious Dogs ◽  
Control Value ◽  
A Value

1. In order to determine if a sustained increase in cardiac output can lead to hypertension, seven conscious dogs were given a continuous infusion of dobutamine, a powerful stimulant of cardiac inotropism, into the left coronary artery for a 7 day period while arterial pressure, cardiac output (electromagnetic flowmeter) and heart rate were measured. 2. The infusion technique (1·5 × 10−8 mol min−1 kg−1, intracoronary) was selected after short-term experiments showed that it increased cardiac output more effectively than intravenous infusion at the same rate. 3. The rise in cardiac output elicited by intracoronary infusion of dobutamine was largest during the first 6 h of the 7 days administration, at which time calculated peripheral resistance was decreased. Subsequently, cardiac output returned progressively toward its control value whereas mean arterial pressure remained elevated (by an average of 20–25 mmHg) and peripheral resistance increased significantly. 4. Measurements of blood and extracellular fluid volumes as well as plasma renin activity indicated that these factors were not involved in the blood pressure increase. 5. When the infusion was ended, arterial pressure fell rapidly but peripheral resistance remained elevated during the first 6 h. Cardiac output fell after 2 and 6 h to a value below that of the pre-infusion control. After 1 day and subsequently, blood pressure became normal, as did the peripheral resistance and cardiac output. 6. Both at the onset and offset transients of this model of hypertension, changes in cardiac output preceded changes in peripheral resistance. These experiments may give experimental support to the concept of cardiogenic hypertension.

Systemic hemodynamics and renal function during long-term pathophysiological increases in circulating endothelin

1995 ◽  
Vol 268 (2) ◽  
pp. R375-R381 ◽  
Author(s):  
F. C. Wilkins ◽  
A. Alberola ◽  
H. L. Mizelle ◽  
T. J. Opgenorth ◽  
J. P. Granger
Keyword(s):  
Renal Function ◽  
Renal Plasma Flow ◽  
Peripheral Resistance ◽  
Plasma Renin ◽  
Chronic Hypertension ◽  
Systemic Hemodynamic ◽  
Endothelin 1 ◽  
Control Value ◽  
Renal Vascular

Although recent studies have reported endogenous plasma endothelin levels to be elevated two- to fivefold in chronic pathophysiological states, whether such an increase in circulating endothelin levels alone can lead to significant long-term alterations in cardiovascular and renal function is not known. The purpose of this study was to examine the long-term systemic hemodynamic and renal effects of a pathophysiological increase in plasma endothelin concentration in chronically instrumented, conscious dogs (n = 7). Infusion of endothelin-1 (2.5 ng.kg-1.min-1) for 8 days increased plasma concentration of immunoreactive endothelin approximately two- to threefold from 6.7 +/- 0.4 to 16.0 +/- 2.2 pg/ml. Mean arterial pressure increased 21% from a control value of 86.7 +/- 2.1 to 105.0 +/- 2.5 mmHg during the endothelin infusion period. Cardiac output averaged 2,200 +/- 205 ml/min during control and fell by 33% on day 4 of endothelin infusion (1,484 +/- 146 ml/min) and was still 14% below control after day 8 of endothelin infusion (1,885 +/- 154 ml/min). Endothelin increased total peripheral resistance from 42.0 +/- 3.1 to 80.3 +/- 9.1 mmHg.l-1.min. Increasing plasma endothelin two- to threefold was associated with an increase in renal vascular resistance and decreases in glomerular filtration rate and renal plasma flow. Endothelin-1 had no long-term effect on plasma renin activity or aldosterone concentration. These data indicate the importance of pathophysiological levels of endothelin in controlling renal and cardiovascular function in chronic conditions. Furthermore, the results indicate that endothelin may play a role as a mediator of chronic hypertension in pathophysiological states associated with endothelial dysfunction.

scholarly journals Nitric oxide may be required to prevent hypertension at the onset of diabetes

2000 ◽  
Vol 279 (4) ◽  
pp. E762-E768 ◽  
Author(s):  
Sharyn M. Fitzgerald ◽  
Michael W. Brands
Keyword(s):  
Nitric Oxide ◽  
Arterial Pressure ◽  
Glomerular Filtration ◽  
Renal Plasma Flow ◽  
Plasma Renin ◽  
Pressure Control ◽  
Progressive Increase ◽  
Onset Of Diabetes ◽  
Regulation Of Vascular Tone

Nitric oxide (NO) plays an important role in the regulation of vascular tone, and evidence suggests that endothelial-dependent relaxation, possibly mediated via NO, is impaired in diabetes. However, the role of the endothelium in arterial pressure control early in diabetes, before dysfunction develops, is not known. This was evaluated in the present study by comparing the responses to induction of diabetes in vehicle-treated rats (D, n = 7) vs. rats chronically treated with N G-nitro-l-arginine methyl ester (l-NAME; D+L, n = 8). A nondiabetic group also was treated with l-NAME (L, n = 7) to control for l-NAME effects over time, independent of diabetes. After baseline measurements, rats were given either vehicle or l-NAME (10 μg · kg−1 · min−1 iv) infusion throughout the experiment. Six days later, streptozotocin (60 mg/kg iv) was administered, followed by a 3-wk diabetic study period. Induction of diabetes in the D+L rats caused a marked and progressive increase in mean arterial pressure throughout the diabetic period, averaging ∼70 mmHg greater than in the D rats and ∼20 mmHg greater than in the L rats. Glomerular filtration rate and renal plasma flow tended to increase during diabetes, but this trend was reversed in the D+L rats. In addition, plasma renin activity increased in the D and D+L rats during week 1 of diabetes but then returned to control in the D rats, while continuing to increase in the D+L rats. These results suggest that, in the early stages of diabetes, NO synthesis is important to prevent hypertension from developing, possibly through actions to maintain glomerular filtration and suppress renin secretion.

Influence of dietary sodium on renin activity and arterial pressure during anesthesia

1976 ◽  
Vol 231 (4) ◽  
pp. 1185-1190 ◽  
Author(s):  
JC Fray ◽  
LG Siwek ◽  
WM Strull ◽  
RN Steller ◽  
JM Wilson
Keyword(s):  
Arterial Pressure ◽  
Enzyme Inhibitor ◽  
Surgical Stress ◽  
Sodium Intake ◽  
Plasma Renin ◽  
Renin Activity ◽  
Dietary Sodium ◽  
Control Value ◽  
Low Sodium ◽  
Anesthetized Dogs

The effect of pentobarbital anesthesia on plasma renin activity (PRA) and mean arterial pressure (MAP) was studied in chronically catheterized dogs maintained on normal or low-sodium intake. Within 1 min of administration, pentobarbital caused a rapid fall in MAP which was followed by a restoration of MAP toward control within 5 min. Thirty minutes after induction of anesthesia, PRA was unchanged in sodium-replete dogs and elevated two-fold in sodium-depleted dogs. MAP was significantly lowered (20 mmHg) in normal salt dogs and only slightly decreased in low-salt dogs 30 min after pentobarbital. MAP returned to preanesthetic control value in dogs given converting enzyme inhibitor before anesthesia. Surgical stress or cutaneous electrical stimulation causey hexamethonium. These results indicate that change in PRA and MAP of pentobarbital-anesthetized dogs is significantly influenced by the sodium intake of the animal and by the degree of surgical stress.

Cardiac output and renal function during insulin hypertension in Sprague-Dawley rats

1996 ◽  
Vol 271 (1) ◽  
pp. R276-R281 ◽  
Author(s):  
M. W. Brands ◽  
W. F. Lee ◽  
H. L. Keen ◽  
M. Alonso-Galicia ◽  
D. H. Zappe ◽  
...  
Keyword(s):  
Heart Rate ◽  
Renal Function ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Insulin Infusion ◽  
Renal Plasma Flow ◽  
Control Period ◽  
Peripheral Resistance ◽  
Sodium Balance ◽  
Control Value

Hyperinsulinemia has been reported to cause hypertension in rats; however, the renal and hemodynamic mechanisms are not known. In this study, changes in renal function, cardiac output (CO), and total peripheral resistance (TPR) were measured during chronic insulin infusion in eight rats (approximately 350 g). After a 4-day control period, a 7-day insulin infusion was begun (1.5 mU.kg-1.min-1 iv), together with glucose (22 mg.kg-1.min-1 iv) to prevent hypoglycemia. Mean arterial pressure (MAP), CO, TPR, and heart rate were measured 24 h/day. MAP increased from 92 +/- 1 to 100 +/- 2 mmHg on day 1 and was 108 +/- 4 mmHg by day 7 of insulin. CO tended to decrease during insulin infusion, although not significantly, averaging 94 +/- 4% of the control value of 121 +/- 7 ml/min. Heart rate did not change significantly from the control value of 384 +/- 8 beats/min. TPR increased significantly to 122 +/- 11% of control by day 7. In five rats, glomerular filtration rate and effective renal plasma flow decreased to 73 +/- 4 and 66 +/- 5% of control, respectively, during insulin. Urinary sodium excretion averaged 2.6 +/- 0.1 and 2.7 +/- 0.1 meq/day during the control and insulin-infusion periods, respectively. These results indicate that insulin hypertension in rats is initiated by an increase in TPR rather than by increased CO. Also, the fact that sodium balance was maintained at elevated arterial pressure suggests that the ability of the kidneys to excrete sodium was impaired chronically during insulin infusion.

Glomerular hemodynamics in severe obesity

2000 ◽  
Vol 278 (5) ◽  
pp. F817-F822 ◽  
Author(s):  
Avry Chagnac ◽  
Talia Weinstein ◽  
Asher Korzets ◽  
Edward Ramadan ◽  
Judith Hirsch ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Arterial Pressure ◽  
Severe Obesity ◽  
Renal Plasma Flow ◽  
Albumin Excretion Rate ◽  
Control Group ◽  
Oral Glucose ◽  
Hydraulic Pressure ◽  
Afferent Arteriole ◽  
Control Value

Differential solute clearances were used to characterize glomerular function in 12 nondiabetic subjects with severe obesity (body mass index >38). Nine healthy subjects served as the control group. In the obese group, glomerular filtration rate (GFR) and renal plasma flow (RPF) exceeded the control value by 51 and 31%, respectively. Consequently, filtration fraction increased. The augmented RPF suggested a state of renal vasodilatation involving, mainly or solely, the afferent arteriole. Albumin excretion rate and fractional albumin clearance increased by 89 and 78%, respectively. Oral glucose tolerance tests were suggestive of insulin resistance. Insulin resistance was positively correlated with GFR ( r = 0.88, P < 0.001) and RPF ( r = 0.72, P < 0.001). Mean arterial pressure was higher than in the control group. Fractional clearances of dextrans of broad size distribution tended to be lowered. The determinants of the GFR were estimated qualitatively by using a theoretical model of dextran transport through a heteroporous membrane. This analysis suggests that the high GFR in very obese subjects may be the result of an increase in transcapillary hydraulic pressure difference (ΔP). An abnormal transmission of increased arterial pressure to the glomerular capillaries through a dilated afferent arteriole could account for the augmentation in ΔP.

Electrical stimulation of the carotid sinus lowers arterial pressure and improves heart rate variability in l-NAME hypertensive conscious rats

2020 ◽  
Vol 43 (10) ◽  
pp. 1057-1067 ◽  
Author(s):  
Gean Domingos-Souza ◽  
Fernanda Machado Santos-Almeida ◽  
César Arruda Meschiari ◽  
Nathanne S. Ferreira ◽  
Camila A. Pereira ◽  
...  
Keyword(s):  
Heart Rate ◽  
Heart Rate Variability ◽  
Electrical Stimulation ◽  
Arterial Pressure ◽  
Carotid Sinus ◽  
Conscious Rats ◽  
Stimulation Of

Influence of right atrial stretch on plasma renin activity in the conscious rat

1987 ◽  
Vol 65 (2) ◽  
pp. 257-259 ◽  
Author(s):  
Susan Kaufman
Keyword(s):  
Plasma Renin Activity ◽  
Superior Vena ◽  
Vena Cava ◽  
Extracellular Fluid ◽  
Plasma Renin ◽  
Renin Activity ◽  
Right Atrial ◽  
Balloon Inflation ◽  
Conscious Rat ◽  
Basal Plasma

Rats were prepared with inflatable balloons at the superior vena cava – right atrium junction. After recovery 1 week later, when blood was taken from conscious, normovolaemic animals plasma renin activity was found not to be influenced by right atrial stretch. Plasma renin activity was then measured in rats in which an extracellular fluid deficit had been produced by peritoneal dialysis against a hyperoncotic, isotonic solution. Although basal plasma renin activity was elevated (6.8 ± 0.9 from 1.5 ± 0.2 ng∙mL∙h, n = 19), no depression was observed in the experimental group after 15 or 90 min of balloon inflation. In rats pretreated with isoprenaline (10 μg/kg body wt.) plasma renin activity was also increased over basal levels, but again balloon inflation caused no reduction in plasma renin activity. It would appear that right atrial stretch has little, if any, influence on renin release in the conscious rat.

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