scholarly journals Acute renal denervation normalizes aortic function and decreases blood pressure in spontaneously hypertensive rats

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Nathalia Juocys Dias Moreira ◽  
Fernando dos Santos ◽  
Edson Dias Moreira ◽  
Daniela Farah ◽  
Leandro Eziquiel de Souza ◽  
...  
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Renal Denervation ◽  
Vascular Reactivity ◽  
Urinary Volume ◽  
Hypertensive Rats ◽  
Response Curves ◽  
Spontaneously Hypertensive ◽  
Functional Changes ◽  
Sham Surgery ◽  
Acute Responses

AbstractMechanisms involved in the acute responses to renal denervation (RDN) have yet to be fully understood. We assessed urinary volume, autonomic control and aorta vascular reactivity after acute RDN. Male normotensive Wistar rats and spontaneously hypertensive rats (SHR) were divided into normotensive + RDN (ND) or sham surgery (NS), and hypertensive + RDN (HD) or sham surgery (HS). Metabolic parameters and hemodynamic measurements were recorded 72h and 4 days after intervention, respectively. Aortic rings were studied 7 days post RDN in an isometric myograph. Concentration–response curves to phenylephrine, sodium nitroprusside and acetylcholine (10–10–10−5 M) were performed. Two-way ANOVA was used for group comparisons and differences reported when p < 0.05. Results are presented as mean ± SEM. Urinary volume was 112% higher in HD vs. HS (HS = 14.94 ± 2.5 mL; HD = 31.69 ± 2.2 mL) and remained unchanged in normotensive rats. Systolic BP was lower in HD rats (HS = 201 ± 12 vs. HD = 172 ± 3 mmHg) without changes in normotensive group. HD group showed increased HF and LF modulation (HS = 5.8 ± 0.7 ms2vs. HD = 13.4 ± 1.4 ms2; HS = 3.5 ± 0.7 ms2vs. HD = 10.5 ± 1.7 ms2, respectively). RDN normalized vascular reactivity in HD rats and increased phenylephrine response in ND rats. Acute fall in BP induced by RDN is associated with increased urinary volume, which in turn may also have contributed to functional changes of the aorta.

Studies on the Role of Sodium-Potassium-Activated ATPase as Determinant of Vascular Reactivity in Wistar-Kyoto and Spontaneously Hypertensive Rats

1980 ◽  
Vol 59 (s6) ◽  
pp. 187s-189s ◽  
Author(s):  
G. Gouthberg ◽  
B. Jandhyala ◽  
B. Folkow
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Vascular Reactivity ◽  
Sodium Pump ◽  
Hypertensive Rats ◽  
Response Curves ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto Rats ◽  
Wistar Kyoto ◽  
Sodium Pump Inhibition

1. The role of Na+-K+-activated ATPase in the regulation of resistance vessel reactivity to barium chloride and noradrenaline was investigated with a pair-perfused hindquarter technique in spontaneously hypertensive rats and Wistar-Kyoto rats (6 and 12 week old). Ouabain (10−4 mol/l) was used to inhibit the sodium pump. 2. In all groups studied, dose-response curves to agonists were shifted to the left when ouabain was added to the perfusion medium. This potentiation in vascular reactivity produced by ouabain was expressed as ‘index for sodium-pump inhibition’ (ISPI = ED50 of an agonist/ED50 + ouabain). 3. In mature rats index for sodium-pump inhibition calculated for both agonists was significantly greater in spontaneously hypertensive rats in comparison with Wistar-Kyoto rats, but not so in young spontaneously hypertensive rats. There was, however, a trend towards increased noradrenaline sensitivity in spontaneously hypertensive rats although the difference from Wistar-Kyoto rats was not statistically significant. 4. The data may suggest that there is some increase in the activity of the sodium pump in the resistance vessels of mature spontaneously hypertensive rats, perhaps to compensate for an increased passive sodium permeability.

scholarly journals Open-loop analysis on sympathetically mediated arterial pressure and urine output responses in spontaneously hypertensive rats: effect of renal denervation

2021 ◽  
Vol 71 (1) ◽  
Author(s):  
Toru Kawada ◽  
Takuya Nishikawa ◽  
Satoru Suehara ◽  
Satoshi Sawada ◽  
Tetsuo Tanaka ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Urine Output ◽  
Spontaneously Hypertensive Rats ◽  
Renal Denervation ◽  
Sympathetic Innervation ◽  
Urine Flow ◽  
Hypertensive Rats ◽  
Loop Analysis ◽  
Intact Side ◽  
Spontaneously Hypertensive

AbstractPrimary acute sympathetic activation (PASA) causes a subsequent arterial pressure (AP) elevation. In this case, an antidiuretic effect via the renal innervation and pressure diuresis can act antagonistically on the kidneys. We examined the effect of PASA on urine output in spontaneously hypertensive rats (SHR) 4–7 days after unilateral renal denervation (RDN) (n = 9). The slope of the plot of urine flow versus AP was positive (0.120 ± 0.031 μL min−1 kg−1 mmHg−1) on the intact side, but it was less than 1/3 of the slope observed previously in normotensive Wistar–Kyoto rats (WKY). RDN did not normalize the slope of urine flow versus AP (0.179 ± 0.025 μL min−1 kg−1 mmHg−1, P = 0.098 versus the intact side). The urine flow at the operating point of the AP tended to be greater on the denervated than the intact side (29.0 ± 1.8 vs. 25.3 ± 1.9 μL min−1 kg−1, P = 0.055). The percent increase (17.2 ± 7.2%) was not different from that observed previously in WKY. Although high-resting sympathetic nerve activity is prerequisite for maintaining hypertension in SHR, the effect of sympathetic innervation on the urine output function was not greater than that in WKY.

Effects of high-cholesterol and atherogenic diets on vascular relaxation in spontaneously hypertensive rats

1997 ◽  
Vol 273 (2) ◽  
pp. H647-H654 ◽  
Author(s):  
M. Cappelli-Bigazzi ◽  
S. Rubattu ◽  
C. Battaglia ◽  
R. Russo ◽  
I. Enea ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Function ◽  
Spontaneously Hypertensive Rats ◽  
Vascular Reactivity ◽  
Male Rats ◽  
Standard Diet ◽  
High Cholesterol ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Endothelium Dependent Relaxation

Hypercholesterolemia is associated with more rapid development of atherosclerosis, and hypertension is frequently associated with abnormal vascular function. Therefore, to investigate the role of hypercholesterolemia and hypertension on vascular function, we studied three groups of male rats (aged 6 wk): normotensive Wistar-Kyoto rats (WKY) as a control group and spontaneously hypertensive rats (SHR) receiving either standard diet (SD; SHR-SD) or high-cholesterol (1%) diet (ChD; SHR-ChD). Vascular reactivity was tested on isolated aortic rings at 4 wk and at 3 and 6 mo of diet. At 3 mo, endothelium-dependent relaxation to acetylcholine (ACh) and ADP was significantly reduced in SHR-ChD but not in SHR-SD compared with WKY. At 6 mo, relaxations to ACh were further impaired in both SHR groups compared with WKY. Endothelium-independent vasodilation to nitroglycerin (NTG) was not different in the three groups of animals throughout 6 mo of diet. In additional experiments, we evaluated vascular reactivity in rats fed with ChD enriched with an excess of vitamin D [atherogenic diet (AD)] capable of producing vascular atherosclerotic lesions. In particular, we studied three additional groups of WKY and SHR rats fed with SD, AD, or AD plus a nonhypotensive dose of the calcium antagonist nitrendipine (Nit). Vasodilation to ACh and ADP was significantly blunted in WKY-AD compared with WKY-SD, whereas it was partially improved in WKY-Nit. There were no differences in endothelium-independent relaxation to NTG in the three WKY groups. In contrast, SHR-AD showed a marked reduction of endothelium-dependent and -independent vasodilation, but only endothelium-dependent vasodilation was preserved by addition of Nit to the diet. These data suggest that the development of vascular dysfunction in rat genetic hypertension is accelerated by ChD, in absence of detectable vascular lesions. Our study also shows that AD alters both vascular smooth muscle and endothelium-dependent relaxation. Low doses of Nit partially preserve endothelium-dependent vasodilation but do not affect the impairment of smooth muscle function in these rats.

Alterations in renal vascular resistance and reactivity in spontaneous hypertension of rats

1980 ◽  
Vol 238 (3) ◽  
pp. H287-H293 ◽  
Author(s):  
K. H. Berecek ◽  
U. Schwertschlag ◽  
F. Gross
Keyword(s):  
Vascular Resistance ◽  
Dose Response ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Response Curves ◽  
Renal Vasculature ◽  
Spontaneously Hypertensive ◽  
Wky Rats ◽  
Dose Response Curves ◽  
Renal Vascular

Vascular resistance and reactivity were investigated in isolated, constant flow perfused kidneys of stroke-prone spontaneously hypertensive rats (SHRSP) and age- and sex-matched normotensive Wistar-Kyoto control rats (WKY rats). Stroke-prone spontaneously hypertensive rats were studied at 4 wk, 2 mo, and 4 mo of age representing different stages of development of hypertension. Resistance in maximally vasodilated vascular beds was greater and the pressure-flow relationship was significantly shifted to the left in kidneys of SHRSP as compared to WKY rats. Responses to norepinephrine, vasopressin, serotonin, and angiotensin II were enhanced in the renal vascular bed of SHRSP. Dose-response curves were shifted to the left, had steeper slopes, decreased thresholds, and increased maximal responses. With longer duration of hypertension, resistance increased, the slopes of the dose-response curves were steeper, and maximum responses greater. The higher resistance and enhanced reactivity in the renal vasculature of SHRSP, already demonstrable in the prehypertensive stage appear to be due to primary structural and functional alterations of the resistance vessels.

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