Adrenaline Neurons and PNMT Activity in the Brain and Spinal Cord of Genetically Hypertensive Rats and Rats with DOCA—salt Hypertension

1981 ◽  
Vol 61 (s7) ◽  
pp. 219s-221s ◽  
Author(s):  
J. P. Chalmers ◽  
P. R. C. Howe ◽  
Y. Wallmann ◽  
I. Tumuls
Keyword(s):  
Spinal Cord ◽  
Spontaneously Hypertensive Rat ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Hypertensive Rat ◽  
Genetically Hypertensive Rats ◽  
Salt Hypertension ◽  
Old Rats ◽  
Wistar Kyoto ◽  
Genetically Hypertensive

1. We have studied the number of phenylethanolamine-N-methyltransferase (PNMT)-containing nerve cells in the medulla and the activity of PNMT in the medulla, spinal cord and hypothalamus of the rat. 2. At 4 weeks of age there was an increase in the number of PNMT cells counted in the medulla of the spontaneously hypertensive rat (SHR; 21%, P < 0.01) and the stroke-prone spontaneously hypertensive rat (SHR-SP; 22%, P < 0.01) compared with the Wistar-Kyoto (WKY) control rat. 3. At 4 months of age there were no significant differences in the number of medullary PNMT cells in two normotensive strains (WKY and Fisher rats), two genetically hypertensive strains (SHR and SHR-SP) and in DOCA-salt hypertensive rats. 4. In four week old rats the activity of PNMT was increased by about 50% in the spinal cord and medulla of the SHR and SHR-SP compared with the WKY rats, and immunotitration experiments suggest that this is due to an increased concentration of enzyme. 5. At 4 months of age there were no increases in PNMT activity of either genetically hypertensive rats or DOCA-salt hypertensive rats.

Intrathecal PACAP-38 causes increases in sympathetic nerve activity and heart rate but not blood pressure in the spontaneously hypertensive rat

2011 ◽  
Vol 300 (1) ◽  
pp. H214-H222 ◽  
Author(s):  
Melissa M. J. Farnham ◽  
Melissa A. Inglott ◽  
Paul M. Pilowsky
Keyword(s):  
Blood Pressure ◽  
Spinal Cord ◽  
Spontaneously Hypertensive Rat ◽  
Sympathetic Tone ◽  
Ventrolateral Medulla ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Hypertensive Rat ◽  
Wistar Kyoto ◽  
Intrathecal Infusion

The rostral ventrolateral medulla contains presympathetic neurons that project monosynaptically to sympathetic preganglionic neurons (SPN) in the spinal cord and are essential for the tonic and reflex control of the cardiovascular system. SPN directly innervate the adrenal medulla and, via postganglionic axons, affect the heart, kidneys, and blood vessels to alter sympathetic outflow and hence blood pressure. Over 80% of bulbospinal, catecholaminergic (C1) neurons contain pituitary adenylate cyclase-activating polypeptide (PACAP) mRNA. Activation of PACAP receptors with intrathecal infusion of PACAP-38 causes a robust, prolonged elevation in sympathetic tone. Given that a common feature of most forms of hypertension is elevated sympathetic tone, this study aimed to determine in the spontaneously hypertensive rat (SHR) and the Wistar Kyoto rat (normotensive control) 1) the proportion of C1 neurons containing PACAP mRNA and 2) responsiveness to intrathecal PACAP-38. We further investigated whether intrathecal infusion of the PACAP antagonist, PACAP(6–38), reduces the hypertension in the SHR. The principal findings are that 1) the proportion of PACAP mRNA-containing C1 neurons is not different between normotensive and hypertensive rats, 2) intrathecal PACAP-38 causes a strain-dependent, sustained sympathoexcitation and tachycardia with variable effects on mean arterial pressure in normotensive and hypertensive rats, and 3) PACAP(6–38) effectively attenuated the effects of intrathecal PACAP-38, but had no effect alone, on any baseline variables. This finding indicates that PACAP-38 is not tonically released in the spinal cord of rats. A role for PACAP in hypertension in conscious rats remains to be determined.

Characterization of renal aldosterone receptors in genetically hypertensive rats

1993 ◽  
Vol 264 (2) ◽  
pp. F286-F291 ◽  
Author(s):  
M. Horiuchi ◽  
H. Nishiyama ◽  
J. Hama ◽  
T. Takenaka ◽  
H. Kondo ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Urine Volume ◽  
Plasma Aldosterone ◽  
Type I ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Receptor Complexes ◽  
Genetically Hypertensive Rats ◽  
Wistar Kyoto ◽  
Genetically Hypertensive

To investigate the aldosterone responsiveness of genetically hypertensive rats, we compared characteristics of renal cytosolic aldosterone receptors from the M strain of stroke-prone, spontaneously hypertensive rats (M-SHRSP) with normotensive Wistar-Kyoto rats (WKY). In M-SHRSP, blood pressure was elevated significantly at 6 wk of age, when their plasma aldosterone concentrations were similar to those in WKY. Decreases in urine volume and sodium excretion were also observed in M-SHRSP. At 10 wk of age, M-SHRSP plasma aldosterone concentrations became significantly higher than those in WKY. On the other hand, the concentration of renal cytosolic aldosterone receptors (type I, aldosterone specific) had already increased at 6 wk of age in M-SHRSP, with no difference in affinity, and levels remained increased thereafter. There were no significant differences in molecular weights or ionic charges of either "activated" or "non-activated" aldosterone-receptor complexes between M-SHRSP and WKY, indicating that the molecular properties were similar in both groups. These results suggest that the increased concentration of aldosterone receptors in the kidneys of M-SHRSP might increase their aldosterone responsiveness and contribute to the development of high blood pressure in these animals.

Overflow of endogenous norepinephrine from PVH nucleus of DOCA-salt hypertensive rats

1995 ◽  
Vol 268 (4) ◽  
pp. H1549-H1554 ◽  
Author(s):  
J. M. Qualy ◽  
T. C. Westfall
Keyword(s):  
Sodium Nitroprusside ◽  
Genetic Model ◽  
Spontaneously Hypertensive Rat ◽  
Tap Water ◽  
Sprague Dawley ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Sd Rats ◽  
Salt Hypertension ◽  
Wistar Kyoto

Previous studies from this laboratory demonstrated that there was enhanced basal and evoked (K+ depolarization) overflow of endogenous norepinephrine (NE) into the perfusate of a push-pull cannula placed in the paraventricular nucleus of the hypothalamus (PVH) of conscious freely moving spontaneously hypertensive rat (SHR) compared with Wistar-Kyoto (WKY) or Sprague-Dawley (SD) rats. The present study was carried out to determine whether results obtained with SHR were specific to this genetic model of hypertension by examining NE release in deoxycorticosterone acetate (DOCA)-salt hypertension. DOCA-salt hypertension was produced in 8-wk-old uninephrectomized SD rats by administering a 50-mg DOCA Silastic pellet subcutaneously 7 days postnephrectomy and providing 0.9% NaCl + 0.2% KCl drinking solution at libitum for 3 wk. Sham-implanted animals received normal tap water. Blood pressure was similar to that of 8- to 10-wk-old SHR. Basal release of NE as well as release after K+ added to the push-pull cannula or sodium nitroprusside or phenylphrine administered intravenously was determined. It was observed that there was no difference in basal overflow or after K+ administration in DOCA-salt hypertensive rats compared with sham animals. Similarly, the increase in NE overflow due to sodium nitroprusside or the decrease due to phenylphrine was similar between DOCA-salt rats or sham controls. This was in sharp contrast to what was observed in SHR: basal or K(+)-evoked release was significantly greater in SHR than WKY, SD, DOCA-salt, or DOCA-sham controls. It is concluded that central noradrenergic activity involving the PVH is not altered in DOCA-salt hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)

Increased Presynaptic α-Adrenoceptor-Mediated Regulation of Noradrenaline Release in the Isolated Perfused Kidney of Spontaneously Hypertensive Rats

1982 ◽  
Vol 63 (s8) ◽  
pp. 309s-311s ◽  
Author(s):  
R. D. Ekas ◽  
M. L. Steenberg ◽  
M. F. Lokhandwala
Keyword(s):  
Nerve Stimulation ◽  
Noradrenaline Release ◽  
Spontaneously Hypertensive Rats ◽  
Spontaneously Hypertensive Rat ◽  
Hypertensive Rats ◽  
Isolated Perfused Kidney ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto Rats ◽  
Hypertensive Rat ◽  
Wistar Kyoto

1. Release of [3H]noradrenaline during peri-arterial nerve stimulation and its inhibition by the presynaptic α-adrenoceptor mechanism were studied in the isolated perfused kidney from spontaneously hypertensive and Wistar-Kyoto rats. 2. A frequency related vasoconstriction as well as [3H]noradrenaline release were observed over the stimulating range of 0.25-32 Hz in both the Wistar-Kyoto and spontaneously hypertensive rats. The spontaneously hypertensive rat kidneys exhibited both an increased vasoconstrictor response and a greater [3H]noradrenaline release when compared with the Wistar-Kyoto rat kidneys. 3. Presynaptic inhibition of [3H]noradrenaline release was evaluated at 2 Hz by using the α-adrenoceptor agonist, tramazoline. Increasing concentrations of tramazoline from 2 × 10−9 mol/l to 2 × 10−7 mol/l caused a dose-dependent decrease in the stimulus-induced release of [3H]noradrenaline in spontaneously hypertensive rats but not in Wistar-Kyoto rats. Only 2 × 10−7 mol/l tramazoline had an inhibitory effect in the Wistar-Kyoto rats. 4. These data indicate that noradrenaline release during sympathetic nerve stimulation is greater in the spontaneously hypertensive rat. The supersensitivity of presynaptic α-adrenoceptors observed in spontaneously hypertensive rats may be a consequence of the greater noradrenaline release present in these animals.

Renal and Vascular Wall Prostaglandins in Spontaneously Hypertensive Rats

1982 ◽  
Vol 63 (s8) ◽  
pp. 253s-255s ◽  
Author(s):  
Yukio Ozawa ◽  
Keika Kan ◽  
Konosuke Konishi ◽  
Waichi Kitajima ◽  
Yasuo Matsumura
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Aortic Wall ◽  
Spontaneously Hypertensive Rat ◽  
Prostaglandin E ◽  
Prostaglandin I2 ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Medullary Tissue ◽  
Hypertensive Rat ◽  
Wistar Kyoto

1. Renal cortical and medullary tissue and aortic wall were removed from spontaneously hypertensive rats and from age-matched Wistar-Kyoto control animals at ages 30, 60, 90 and 120 days. The tissues were incubated and the release of prostaglandins into the incubation medium was measured. 2. Compared with Wistar-Kyoto control animals, the release of prostaglandin E from renal medullary tissue in spontaneously hypertensive rats was raised at 30 days (pre-hypertensive stage) and 90 days (early hypertensive stage), but decreased later with further establishment of hypertension. No such trend was seen with renal cortical tissue. Tissue release of prostaglandin F tended to be generally high in the spontaneously hypertensive rats compared with that in the control animals, but the difference was not significant. 3. The release of prostaglandin I2, as indicated by measurements of 6-keto prostaglandin F1α, from aortic wall tissue in the spontaneously hypertensive rat during its pre-hypertensive and early hypertensive stages was similar to values obtained in the age-matched control animal. However, aortic wall prostaglandin I2 release in spontaneously hypertensive rats increased thereafter, and was significantly raised at 90 and 120 days. No similar trend was observed with thromboxan A2 release. Release of prostaglandin I2 and thromboxan A2 from renal tissues in spontaneously hypertensive rats did not differ significantly from that in control animals. 4. It is suggested that indomethacin-induced aggravation of hypertension in the spontaneously hypertensive rat may result from suppression of aortic wall prostaglandin I2 formation rather than from the suppression of renal prostaglandin E2 production.

Enhanced Phospholipase A2 Activity in Cultured Cardiomyocytes from Newborn Spontaneously Hypertensive Rat

1996 ◽  
Vol 90 (5) ◽  
pp. 403-407
Author(s):  
Elisabeth Millanvoye-Van Brussel ◽  
Marie-Aude Devynck
Keyword(s):  
Phospholipase A2 ◽  
Spontaneously Hypertensive Rat ◽  
Hypertensive Rats ◽  
Rat Cardiomyocytes ◽  
Spontaneously Hypertensive ◽  
Hypertensive Rat ◽  
Wistar Kyoto Rat ◽  
Wistar Kyoto ◽  
Phospholipase A2 Activity ◽  
Cultured Cardiomyocytes

1. Changes in membrane lipid composition and metabolism could participate in myocardial membrane dysfunction in essential or experimental hypertension. Phospholipid-bound fatty acid profile and metabolism are altered in cultured heart myocytes of newborn genetically hypertensive rats. The present study was designed to investigate the participation of phospholipase A2 in these modifications. 2. Phospholipase A2 activity of cultured cardiomyocytes of neonate spontaneously hypertensive rats and normotensive control Wistar—Kyoto rats was compared. The enzyme activity was measured using 2-[1-14C]arachidonyl-phosphatidylethanolamine as substrate. In both strains, Ca2+-dependent and independent phospholipase A2 activities were present. Only the Ca2+-dependent enzyme activity was altered in spontaneously hypertensive rat cardiomyocytes. With 0.2 mmol/l substrate and 5 mmol/l Ca2+, the phospholipase A2 activities were 79.0 ± 13.4 and 26.0 ± 3.6 nmol h−1 mg−1 of protein in spontaneously hypertensive and Wistar—Kyoto rat cardiomyocytes respectively (n = 10 in both cases, P = 0.001). The maximum velocity of the enzyme was three times higher in spontaneously hypertensive rat than in Wistar—Kyoto rat, without changes in the apparent affinity of the enzyme for its substrate. 3. The present results demonstrate an enhanced phospholipase A2 activity in cultured heart muscle cells of spontaneously hypertensive rats, which could be genetically determined.

scholarly journals Sympathetic Nerve Activity and Baroreflex are Strongly Altered in a Context of Severe Hypertension Using the Spontaneously Hypertensive Rat Model Associated with Chronic Reduction of Nitric Oxide

2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Christine Vayssettes-Courchay ◽  
Jonathan Melka ◽  
Clothilde Philouze ◽  
Najah Harouki
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Spontaneously Hypertensive Rat ◽  
Severe Hypertension ◽  
Temporal Correlation ◽  
Hypertensive Rats ◽  
Nerve Activity ◽  
Spontaneously Hypertensive ◽  
Hypertensive Rat ◽  
Wistar Kyoto

The aim of our study is to investigate the sympathetic output and baroreflex via renal sympathetic nerve activity (RSNA) recording in a model of severe hypertension which exhibits arterial, cardiac, and renal damages, the spontaneously hypertensive rat (SHR) under lowered NO bioavailability. SHR are treated from 18 to 20 weeks of age with a low dose of L-NAME, a NO synthase inhibitor, in drinking water (SHRLN) and compared to SHR and normotensive Wistar Kyoto (WKY) rats. After the two-week treatment, rats are anesthetized for RSNA, mean blood pressure (MBP), and heart rate (HR) recording. MBP is higher in SHR than in WKY and higher in SHRLN than in SHR. Compared to WKY, SHR displays an alteration in the baroreflex with a displacement of the sympathoinhibition curve to highest pressures; this displacement is greater in SHRLN rats. The bradycardic response is reduced in SHRLN compared to both SHR and WKY. In hypertensive rats, SHR and SHRLN, basal RSNA is modified, the maximal amplitude of burst is reduced, but minimal values are increased, indicating an increased basal RSNA with reduced bursting activity. The temporal correlation between RSNA and HR is preserved in SHR but altered in 10 SHRLN out of 10. The RSNA inhibition triggered by the Bezold–Jarisch reflex activation is not modified in hypertensive rats, SHR or SHRLN, in contrast to that triggered by the baroreflex. Histological analysis of the carotid bifurcation does not reveal any abnormality in SHRLN at the level of the carotid sinus. In conclusion, data indicate that the sympathetic outflow is altered in SHRLN with a strong reduction of the baroreflex sympathoinhibition and suggest that its central pathway is not involved. These additional results on SHRLN also confirm the usefulness of this model of severe hypertension with multiple target organ damages.

Enhanced renal sensitivity of the spontaneously hypertensive rat to urotensin II

2008 ◽  
Vol 295 (4) ◽  
pp. F1239-F1247 ◽  
Author(s):  
Alaa E. S. Abdel-Razik ◽  
Richard J. Balment ◽  
Nick Ashton
Keyword(s):  
Renal Function ◽  
Spontaneously Hypertensive Rat ◽  
Renal Medulla ◽  
Fractional Excretion ◽  
Urotensin Ii ◽  
Spontaneously Hypertensive ◽  
Wky Rats ◽  
Hypertensive Rat ◽  
Fractional Excretion Of Sodium ◽  
Wistar Kyoto

Urotensin II (UII) has been implicated widely in cardiovascular disease. The mechanism(s) through which it contributes to elevated blood pressure is unknown, but its emerging role as a regulator of mammalian renal function suggests that the kidney might be involved. The aim of this study was to determine the effect of UII on renal function in the spontaneously hypertensive rat (SHR). UII infusion (6 pmol·min−1·100 g body wt−1) in anesthetized SHR and control Wistar-Kyoto (WKY) rats produced marked reductions in glomerular filtration rate (ΔGFR WKY, n = 7, −0.3 ± 0.1 vs. SHR, n = 7, −0.6 ± 0.1 ml·min−1·100 g body wt−1, P = 0.03), urine flow, and sodium excretion rates, which were greater in SHR by comparison with WKY rats. WKY rats also showed an increase in fractional excretion of sodium (ΔFENa; +0.6 ± 0.1%, P = 0.02) in contrast to SHR in which no such change was observed (ΔFENa −0.6 ± 0.2%). Blockade of the UII receptor (UT), and thus endogenous UII activity, with urantide evoked an increase in GFR which was greater in SHR (+0.3 ± 0.1) compared with WKY rats (+0.1 ± 0.1 ml·min−1·100 g body wt−1, P = 0.04) and was accompanied by a diuresis and natriuresis. UII and UT mRNA expression were greater in the renal medulla than the cortex of both strains; however, expression levels were up to threefold higher in SHR tissue. SHR are more sensitive than WKY to UII, which acts primarily to lower GFR thus favoring salt retention in this model of hypertension.

Hypoxic moderation of systemic hypertension in the spontaneously hypertensive rat

1987 ◽  
Vol 252 (3) ◽  
pp. R554-R561 ◽  
Author(s):  
W. N. Henley ◽  
A. Tucker
Keyword(s):  
Blood Pressure ◽  
Spontaneously Hypertensive Rat ◽  
Metabolic Adaptation ◽  
Systemic Hypertension ◽  
Thyroid Status ◽  
Blood Pressure Elevation ◽  
Spontaneously Hypertensive ◽  
Moderate Hypobaric Hypoxia ◽  
Hypertensive Rat ◽  
Wistar Kyoto

The mechanism by which chronic, moderate, hypobaric hypoxia attenuates systemic systolic blood pressure (SBP) in the spontaneously hypertensive rat (SHR) was investigated in a three-part study. In experiment 1, 10 wk of hypoxia (3,658 m altitude) commencing in 7-wk-old rats was partially effective in preventing the rise in SBP [hypoxic SHR (SHR-H) 154 mmHg vs. normoxic SHR (SHR-N) 180 mmHg; P less than 0.01]. When hypoxia was initiated in 5-wk-old SHR (experiments 2 and 3), protection against hypertension was nearly complete (experiment 2: SHR-H 122 mmHg vs. SHR-N 175 mmHg; P less than 0.001; experiment 3: 135 vs. 152 mmHg, respectively; P less than 0.05). Elevations in O2 consumption (VO2) and rectal temperature (Tre) in SHR vs. normotensive [Wistar-Kyoto (WKY)] rats provided evidence that the SHR is a hypermetabolic animal. Thyroid hormonal indices suggested that SHR changed from a low to high thyroid status at a time that rapid blood pressure elevation occurred; however, hypoxia did not influence thyroid status. Acute, significant decrements in VO2 and Tre in SHR-H (experiments 2 and 3) accompanied the attenuation of SBP by hypoxia, whereas large decrements in VO2 and SBP did not occur in hypoxic WKY. Timely administration of moderate hypoxia protects against the development of hypertension in the SHR. This protection may relate to a metabolic adaptation made by the hypoxic SHR.

Effect of dietary potassium chloride in borderline hypertensive rats.

1992 ◽  
Vol 3 (2) ◽  
pp. 188-195
Author(s):  
G F DiBona ◽  
S Y Jones
Keyword(s):  
Sodium Chloride ◽  
Environmental Stress ◽  
Potassium Chloride ◽  
Spontaneously Hypertensive Rat ◽  
Dietary Sodium ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Hypertensive Rat ◽  
Dietary Potassium ◽  
Sodium Chloride Intake

The borderline hypertensive rat is the first filial offspring of the spontaneously hypertensive rat and the Wistar-Kyoto rat. With increased dietary sodium chloride intake, the borderline hypertensive rat develops hypertension and exaggerated cardiovascular and renal responses to acute environmental stress, similar to those observed in the hypertensive spontaneously hypertensive rat parent. In other models of sodium chloride-sensitive hypertension with different genetic background (Dahl rat), dietary potassium chloride supplementation protects against the development of hypertension, increased sympathetic nervous system activity, and exaggerated responses to acute environmental stress. This investigation sought to determine whether the dietary sodium chloride-induced development of both the hypertension and the exaggerated responses to acute environmental stress could be reversed or prevented by increased dietary potassium chloride intake. Dietary potassium chloride intake was increased with a 1% potassium chloride drinking solution either after 12 wk of 8% sodium chloride intake (reversal) or concomitant with the onset of 12 wk of 8% sodium chloride intake (prevention). An increase in dietary potassium chloride intake did not reverse or prevent the development of either the hypertension or the exaggerated cardiovascular and renal responses to acute environmental stress in borderline hypertensive rats fed 8% sodium chloride. It is concluded that the difference in genetic background between borderline hypertensive rats and other models of sodium chloride-sensitive hypertension is an important determinant of the protective effect of dietary potassium chloride supplementation.

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