Effect of afferent renal nerve stimulation on blood pressure, heart rate and noradrenergic activity in conscious rats

1986 ◽  
Vol 17 (2) ◽  
pp. 121-130 ◽  
Author(s):  
K.P. Patel ◽  
M.M. Knuepfer
1986 ◽  
Vol 251 (5) ◽  
pp. R867-R877
Author(s):  
N. L. Herman ◽  
D. R. Kostreva

The reflex effects of renal afferents on the heart were studied in pentobarbital-anesthetized rats (400-425 g) using 2-[14C]deoxyglucose (DG). Three groups of rats were given a single bolus injection of DG (100 mu Ci/kg) 1) six controls, 2) four with periodic electrical stimulation of the proximal end of a cut renal nerve (2 Hz, 0.5-ms width) and 1-mA current, and 3) six with intermittent renal venous occlusion (unilateral). Forty-five minutes after injection the heart was removed, cooled quickly, and frozen-sectioned. Sections 20 micron thick were exposed to film for 12 days. The resulting autoradiographs were scanned using a computerized densitometer, and these densities were converted to relative glucose utilization (GlU, mumol X 100 g-1 X min-1) using the lumped constant for rat brain. Both renal venous occlusion and renal afferent nerve stimulation resulted in a decrease in blood pressure of 6.7 +/- 0.6 mmHg (P less than 0.001) and 7.3 +/- 0.7 mmHg (P less than 0.001) and heart rate-blood pressure product of 5.6 +/- 0.7% (P less than 0.001) and 8.8 +/- 0.8% (P less than 0.001), respectively, and afferent renal nerve stimulation induced a decrease in heart rate of 7.2 +/- 0.9 beats/min (P less than 0.01). However, when compared with control, renal venous occlusion induced a significant increase in GlU in left ventricular myocardium (LV myo, P less than 0.05), endocardium (LV endo, P less than 0.001), and papillary muscle (LV pap, P less than 0.001), whereas afferent renal nerve stimulation induced a significant increase in GlU in LV endo (P less than 0.05) and LV pap (P less than 0.002) only. This study shows both a reflex increase in GlU for the rat heart and a decrease in heart rate with either renal vein occlusion or afferent renal nerve stimulation.


Hypertension ◽  
2016 ◽  
Vol 67 (6) ◽  
pp. 1211-1217 ◽  
Author(s):  
Mark R. de Jong ◽  
Annemiek F. Hoogerwaard ◽  
Pim Gal ◽  
Ahmet Adiyaman ◽  
Jaap Jan J. Smit ◽  
...  

Hypertension ◽  
2016 ◽  
Vol 68 (3) ◽  
pp. 707-714 ◽  
Author(s):  
Mark R. de Jong ◽  
Ahmet Adiyaman ◽  
Pim Gal ◽  
Jaap Jan J. Smit ◽  
Peter Paul H.M. Delnoy ◽  
...  

2021 ◽  
Author(s):  
◽  
Anna Francina Hoogerwaard

Worldwide there are many people with hypertension. However, the treatment of high blood pressure is not optimal and in many patients the blood pressure remains too high despite drug therapy. A potential new treatment for hypertension is renal sympathetic denervation (RDN); hereby the sympathetic nerves surrounding the renal arteries are denervated. The first results were promising regarding blood pressure reduction, but the first randomized sham-controlled studies showed disappointing results. Currently, the RDN procedure is under investigation to improve the procedure and select the appropriate hypertension patient category. In this thesis renal nerve stimulation (RNS) before and after renal denervation has been applied to improve the procedure. RNS was used both before and after RDN. Before RDN, RNS causes a rise in blood pressure, this effect is no longer present after RDN. This thesis describes the acute RNS-induced hemodynamic effects and changes in heart rate variability before and after RDN. In addition, we showed that patients who had no RNS-induced blood pressure increase after RDN had much better blood pressure lowering at follow-up compared to the patients who still had RNS-induced blood pressure rise. RNS may thus potentially be used to determine whether the denervation is complete. In addition, we describe in the thesis the possible future applications of RDN in other cardiovascular diseases characterized by sympathetic overdrive. Further research into the exact role of renal nerve stimulation during RDN is necessary, but this thesis has provided insight into the possible underlying mechanism of both RDN and RNS.


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