Decreased hexokinase activity in paraventricular nucleus of adult SHR and renal hypertensive rats

1988 ◽  
Vol 254 (3) ◽  
pp. R508-R512 ◽  
Author(s):  
T. L. Krukoff
Keyword(s):  
Arterial Pressure ◽  
Paraventricular Nucleus ◽  
Metabolic Activity ◽  
Central Nucleus ◽  
Hypothalamic Nucleus ◽  
Sprague Dawley ◽  
Hypertensive Rats ◽  
Medial Nucleus ◽  
Wistar Kyoto ◽  
Renal Hypertensive Rats

Metabolic activity was assessed in the brains of spontaneously hypertensive rats (SHR) using the histochemical hexokinase (HK) technique and photodensitometric analysis. Of eight regions known to play a role in cardiovascular regulation, only the paraventricular nucleus of the hypothalamus (PVH) exhibited alterations in HK activity. Significantly lower levels of HK activity in SHR than in control Sprague-Dawley and Wistar-Kyoto rats were measured in both the parvo- and magnocellular divisions of the PVH. No differences in HK activity were found in the anterior hypothalamic nucleus, posterior hypothalamic nucleus, supraoptic nucleus, subfornical organ, central nucleus of the amygdala, or the medial nucleus of the tractus solitarius of SHR. Similar results were obtained in renal hypertensive rats; furthermore, a positive correlation was found between levels of arterial pressure and densitometric readings. These latter results strongly suggest that metabolic alterations in the PVH of SHR are directly related to the increases in arterial pressure and are not due to the genetic makeup of SHR. In light of studies by others, the data from the present study have been interpreted to suggest that the decreases in metabolic activity in the PVH of the adult SHR are the result of a central attempt to bring the level of the arterial pressure down to normal levels and not to the altered activity of a region that might be acting to keep arterial pressure elevated.

Age-dependent overflow of endogenous norepinephrine from paraventricular hypothalamic nucleus of hypertensive rats

1993 ◽  
Vol 265 (1) ◽  
pp. H39-H46 ◽  
Author(s):  
J. M. Qualy ◽  
T. C. Westfall
Keyword(s):  
Blood Pressure ◽  
Neuronal Activity ◽  
Reciprocal Relationship ◽  
Hypothalamic Nucleus ◽  
Sprague Dawley ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Paraventricular Hypothalamic Nucleus ◽  
Wistar Kyoto ◽  
The Relationship

The relationship between age and central noradrenergic neuronal activity of the paraventricular hypothalamic nucleus (PVH) was examined in 7- to 10-, 12- to 14-, and 30- to 36-wk-old Sprague-Dawley (SD), Wistar-Kyoto (WKY), and spontaneously hypertensive rats (SHR). As an index of noradrenergic activity, endogenous norepinephrine (NE) overflow was assessed utilizing a miniaturized push-pull cannula assembly in unanesthetized freely moving rats. NE overlow under basal, 56 mM K+ stimulation, and in response to pressor/depressor drugs, were examined in all three strains at all ages. Significant increases in basal and K(+)-stimulated overflow of endogenous NE from the PVH were observed in all ages of SHR compared with normotensive controls with the greatest percent increase occurring during the development of hypertension in SHR. In addition, a reciprocal relationship exists with respect to blood pressure and overflow of NE from the PVH such that increases/decreases in blood pressure elicit decreases/increases in NE overflow in all strains at all ages examined. However, developing hypertensive SHR exhibited attenuated decreases in overflow of NE from the PVH compared with age-matched controls and established hypertensive SHR. These results suggest that noradrenergic pathways of the PVH contribute to the development and maintenance of arterial pressure hemostasis and that enhanced central noradrenergic neuronal activity is greatest during the development of hypertension in SHR.

GABA-A Function and Receptor Binding in the Paraventricular Nucleus in Chronic Renal Wrap Hypertension

Hypertension ◽  
2000 ◽  
Vol 36 (suppl_1) ◽  
pp. 701-701
Author(s):  
Joseph R Haywood ◽  
Teresa Craig ◽  
Julie Hensler ◽  
Carmen Hinojosa-Laborde
Keyword(s):  
Arterial Pressure ◽  
Paraventricular Nucleus ◽  
Receptor Binding ◽  
Binding Sites ◽  
Sprague Dawley ◽  
Hypertensive Rats ◽  
Gaba A ◽  
Gaba Binding ◽  
In Vivo Autoradiography

P48 The onset of renal wrap hypertension is associated with a reduced tonic GABA inhibition in the paraventricular nucleus (PVN) on the sympathetic nervous system. This reduced functional inhibition occurs without a change in GABA-A receptor binding in the PVN. The goal of the present study was to determine if GABAergic transmission and GABA binding is altered in chronic renal wrap hypertensive rats. Sprague-Dawley rats were made hypertensive or sham-operated. Four weeks later, animals were prepared with femoral artery catheters for the measurement of arterial pressure. Subgroups were also prepared with bilateral cannulae directed at the PVN. The renal wrap rats had higher mean arterial pressure (MAP): 139±4 mmHg vs.113±2 mmHg, but heart rate (HR) was not different (354±12 bpm vs. 369±6 bpm) as compared to control animals. Administration of the GABA-A antagonist, bicuculline, into the PVN caused a greater increase in MAP and HR in wrap animals (25±2 mmHg and 150±30 bpm) compared to sham operated rats (16±2 mmHg and 89±12 bpm). GABA-A binding sites in the PVN were estimated using in vivo autoradiography. [3H]-Flunitrazepam was used as the receptor ligand. Magnocellular neurons of the PVN showed a higher density of receptors than other areas of the nucleus. However, the number of binding sites was not different between normotensive and hypertensive rats in either the high density (1825±56 vs. 1756±41 fmol/mg protein) or low density (1454±26 vs. 1433±57 fmol/mg protein) regions of PVN. These data indicate that the inhibition by GABA in the PVN is augmented in the chronic stage of hypertension, and appears to be unrelated to a change in the number of GABA binding sites. The increased GABAergic inhibition is in contrast to the reduced inhibition that has been observed during the onset of hypertension.

scholarly journals Further evidence against the role renal medullary perfusion in short-term control of arterial pressure in normotensive and mildly or overtly hypertensive rats

2021 ◽  
Vol 473 (4) ◽  
pp. 623-631
Author(s):  
Bożena Bądzyńska ◽  
Iwona Baranowska ◽  
Janusz Sadowski
Keyword(s):  
Arterial Pressure ◽  
Renal Excretion ◽  
Sodium Concentration ◽  
Sprague Dawley ◽  
Hypertensive Rats ◽  
Critical Determinant ◽  
Human Hypertension ◽  
Pressure Elevation ◽  
Doppler Probe ◽  
Medullary Tissue

AbstractEarlier evidence from studies of rat hypertension models undermines the widespread view that the rate of renal medullary blood flow (MBF) is critical in control of arterial pressure (MAP). Here, we examined the role of MBF in rats that were normotensive, with modest short-lasting pressure elevation, or with overt established hypertension. The groups studied were anaesthetised Sprague-Dawley rats: (1) normotensive, (2) with acute i.v. norepinephrine-induced MAP elevation, and (3) with hypertension induced by unilateral nephrectomy followed by administration of deoxycorticosterone-acetate (DOCA) and 1% NaCl drinking fluid for 3 weeks. MBF was measured (laser-Doppler probe) and selectively increased using 4-h renal medullary infusion of bradykinin. MAP, renal excretion parameters and post-experiment medullary tissue osmolality and sodium concentration were determined. In the three experimental groups, baseline MAP was 117, 151 and 171 mmHg, respectively. Intramedullary bradykinin increased MBF by 45%, 65% and 70%, respectively, but this was not associated with a change in MAP. In normotensive rats a significant decrease in medullary tissue sodium was seen. The intramedullary bradykinin specifically increased renal excretion of water, sodium and total solutes in norepinephrine-treated rats but not in the two other groups. As previously shown in models of rat hypertension, in the normotensive rats and those with acute mild pressure elevation (resembling labile borderline human hypertension), 4-h renal medullary hyperperfusion failed to decrease MAP. Nor did it decrease in DOCA-salt model mimicking low-renin human hypertension. Evidently, within the 4-h observation, medullary perfusion was not a critical determinant of MAP in normotensive and hypertensive rats.

scholarly journals Duration of Electrically Induced Atrial Fibrillation Is Augmented by High Voltage of Stimulus with Higher Blood Pressure in Hypertensive Rats

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Tomomi Nagayama ◽  
Yoshitaka Hirooka ◽  
Akiko Chishaki ◽  
Masao Takemoto ◽  
Yasushi Mukai ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Blood Pressure ◽  
Arterial Pressure ◽  
High Voltage ◽  
Spontaneously Hypertensive Rats ◽  
Low Voltage ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
High Stimulus ◽  
Wistar Kyoto

Objective.Many previous clinical studies have suggested that atrial fibrillation (AF) is closely associated with hypertension. However, the benefits of antihypertensive therapy on AF are still inconsistent, and it is necessary to explore the factors augmenting AF in hypertensive rats. The aim of the present study was to investigate the correlation between arterial pressure or voltage stimulus and to the duration of electrically induced AF in normotensive or hypertensive rats.Methods.AF was reproducibly induced by transesophageal atrial burst pacing in spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). We did the burst pacing at high (20 V) or low (5 V) voltage.Results.Duration of AF did not correlate with systolic blood pressure (SBP) and stimulus voltage in WKY. However, only in SHR, duration of AF with high stimulus voltage significantly correlated with SBP and was significantly longer in high than in low voltage stimulus.Discussion and Conclusion.Duration of AF is augmented by high voltage stimulus with higher blood pressure in SHR.

High-NaCl diets increase natriuretic and diuretic responses in salt-resistant but not salt-sensitive SHR

1991 ◽  
Vol 260 (6) ◽  
pp. F890-F897 ◽  
Author(s):  
M. S. Mozaffari ◽  
S. Jirakulsomchok ◽  
Z. H. Shao ◽  
J. M. Wyss
Keyword(s):  
Arterial Pressure ◽  
Renal Denervation ◽  
Isotonic Saline ◽  
Renal Nerves ◽  
Sprague Dawley ◽  
Volume Loading ◽  
Spontaneously Hypertensive ◽  
Volume Load ◽  
Sprague Dawley Rats ◽  
Wistar Kyoto

This study tested the hypothesis that NaCl-sensitive spontaneously hypertensive rats (SHR-S) display a defect in natriuretic and diuretic responses to acute volume loading that contributes to the rise in arterial pressure observed when the rats are fed a high-NaCl diet. Seven-week-old SHR-S and NaCl-resistant SHR rats (SHR-R) and normotensive (Wistar-Kyoto and Sprague-Dawley rats) were fed high- or basal NaCl diets. After 2.5 wk on the diets, preinstrumented conscious rats received an intravenous infusion (5% body wt; 0.5 ml/min) of isotonic saline, and urine was collected through a bladder catheter for 90 min. Control rats on the high-NaCl diet (compared with basal) excreted a significantly greater percentage of Na+ and volume load. In contrast, SHR-S on high-NaCl diet (compared with basal) had a very small increase in natriuretic response and no increase in diuretic response to volume expansion. The effect of renal denervation on natriuretic and diuretic responses to volume load was tested. In SHR-R on 1 and 8% NaCl diets, renal denervation had little or no effect on these responses, suggesting that renal nerves do not play a prominent role in the dietary NaCl-induced increases in the natriuretic and diuretic responses to volume load. These results demonstrate that NaCl-resistant rats rapidly adapt to diets high in NaCl content with increased natriuretic and diuretic responses to acute volume loading. The failure of SHR-S to adapt to the dietary challenge may result in volume loading and a secondary increase in arterial pressure after feeding.

Functional and structural changes with hypoxia in pulmonary circulation of spontaneously hypertensive rats

1994 ◽  
Vol 77 (3) ◽  
pp. 1101-1107 ◽  
Author(s):  
S. P. Janssens ◽  
B. T. Thompson ◽  
C. R. Spence ◽  
C. A. Hales
Keyword(s):  
Pulmonary Hypertension ◽  
Arterial Pressure ◽  
Vascular Remodeling ◽  
Spontaneously Hypertensive Rats ◽  
Structural Changes ◽  
Chronic Hypoxia ◽  
Acute Hypoxia ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto

Chronic hypoxic pulmonary hypertension involves both vasoconstriction and vascular remodeling. Spontaneously hypertensive rats (SHR) have an increased systemic vascular resistance and a greater responsiveness to constricting stimuli. We hypothesized that, in contrast to age-matched normotensive Wistar-Kyoto rats (WKY), SHR also display spontaneous pulmonary hypertension in normoxia and increased vascular response to acute and chronic hypoxia. Baseline mean pulmonary arterial pressure (PAP) and total pulmonary resistance (TPR) were higher in SHR than in WKY. With acute hypoxia (10% O2 for 15 min), PAP increased to the same extent in SHR and WKY and cardiac output (CO) was unchanged in WKY but increased in SHR. Thus, the rise in PAP in the SHR might be accounted for by the rise in CO, as TPR did not rise, but not that in the WKY, as TPR increased. After 12 days in hypoxia (10% O2), mean arterial pressure was unchanged in WKY but decreased significantly in SHR without a change in CO. PAP increased by 59% in SHR and 54% in WKY when the rats were taken from the hypoxic chamber for 1 h. Acute hypoxic challenge caused a further increase in PAP only in WKY. Medial wall thickness of alveolar duct and terminal bronchial vessels was similar in WKY and SHR after chronic hypoxia. We conclude that SHR exhibit mild baseline pulmonary hypertension in normoxia and that chronic hypoxia does not produce a disproportionate increase in SHR pulmonary vascular remodeling and pulmonary hypertension.

α2-Adrenergic receptors in NTS facilitate baroreflex function in adult spontaneously hypertensive rats

2002 ◽  
Vol 282 (6) ◽  
pp. H2336-H2345 ◽  
Author(s):  
Linda F. Hayward ◽  
Alecia P. Riley ◽  
Robert B. Felder
Keyword(s):  
Arterial Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Baroreflex Control ◽  
Renal Sympathetic Nerve Activity ◽  
Spontaneously Hypertensive ◽  
Aortic Depressor Nerve ◽  
Baroreflex Function ◽  
Wistar Kyoto ◽  
Renal Sympathetic

We examined the effect of α2-adrenoreceptor blockade in the nucleus of the solitary tract (NTS) on baroreflex responses elicited by electrical stimulation of the left aortic depressor nerve (ADN) in urethane-anesthetized spontaneously hypertensive rats (SHR, n = 11) and normotensive Wistar-Kyoto rats (WKY, n = 11). ADN stimulation produced a frequency-dependent decrease in mean arterial pressure (MAP), renal sympathetic nerve activity (RSNA), and heart rate (HR). In SHR, unilateral microinjection of idazoxan into the NTS markedly reduced baroreflex control of MAP, RSNA, and HR and had a disproportionately greater influence on baroreflex control of MAP than of RSNA. In WKY, idazoxan microinjections did not significantly alter baroreflex function relative to control vehicle injections. These results suggest that baroreflex regulation of arterial pressure in SHR is highly dependent on NTS adrenergic mechanisms. The reflex regulation of sympathetic outflow to the kidney is less influenced by the altered α2-adrenoreceptor mechanisms in SHR.

scholarly journals Exercise changes regional vascular control by commissural NTS in spontaneously hypertensive rats

2010 ◽  
Vol 299 (1) ◽  
pp. R291-R297 ◽  
Author(s):  
Cristiana A. Ogihara ◽  
Gerhardus H. M. Schoorlemmer ◽  
Adriana C. Levada ◽  
Tania C. Pithon-Curi ◽  
Rui Curi ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Spontaneously Hypertensive Rats ◽  
The Body ◽  
Swimming Exercise ◽  
Exercise Session ◽  
Hypertensive Rats ◽  
Vascular Control ◽  
Spontaneously Hypertensive ◽  
Wky Rats ◽  
Wistar Kyoto

Inhibition of the commissural nucleus of the solitary tract (commNTS) induces a fall in sympathetic nerve activity and blood pressure in spontaneously hypertensive rats (SHR), which suggests that this subnucleus of the NTS is a source of sympathoexcitation. Exercise training reduces sympathetic activity and arterial pressure. The purpose of the present study was to investigate whether the swimming exercise can modify the regional vascular responses evoked by inhibition of the commNTS neurons in SHR and normotensive Wistar-Kyoto (WKY) rats. Exercise consisted of swimming, 1 h/day, 5 days/wk for 6 wks, with a load of 2% of the body weight. The day after the last exercise session, the rats were anesthetized with intravenous α-chloralose, tracheostomized, and artificially ventilated. The femoral artery was cannulated for mean arterial pressure (MAP) and heart rate recordings, and Doppler flow probes were placed around the lower abdominal aorta and superior mesenteric artery. Microinjection of 50 mM GABA into the commNTS caused similar reductions in MAP in swimming and sedentary SHR (−25 ± 6 and −30 ± 5 mmHg, respectively), but hindlimb vascular conductance increased twofold in exercised vs. sedentary SHR (54 ± 8 vs. 24 ± 5%). GABA into the commNTS caused smaller reductions in MAP in swimming and sedentary WKY rats (−20 ± 4 and −16 ± 2 mmHg). Hindlimb conductance increased fourfold in exercised vs. sedentary WKY rats (75 ± 2% vs. 19 ± 3%). Therefore, our data suggest that the swimming exercise induced changes in commNTS neurons, as shown by a greater enhancement of hindlimb vasodilatation in WKY vs. SHR rats in response to GABAergic inhibition of these neurons.

Norepinephrine levels in paraventricular nucleus of spontaneously hypertensive rats: role of neuropeptide Y

1993 ◽  
Vol 265 (3) ◽  
pp. H893-H898 ◽  
Author(s):  
N. D. Woo ◽  
K. Mukherjee ◽  
P. K. Ganguly
Keyword(s):  
Neuropeptide Y ◽  
Paraventricular Nucleus ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Central Neurons ◽  
Sympathetic Regulation ◽  
Series Of Experiments ◽  
Wistar Kyoto

Recent evidence supports the view that the sympathetic system actively participates in the development of hypertension. Because norepinephrine, contained within central neurons involved in cardiovascular sympathetic regulation, is known to coexist with neuropeptide Y, it is possible that a functional interaction between neuropeptide Y and norepinephrine exists within the brain. In an effort to clarify whether or not central catecholamine systems are modulated by neuropeptide Y in hypertensive situations, the paraventricular nucleus of spontaneously hypertensive rats was exposed to neuropeptide Y (10(-9) M), and levels of norepinephrine were sampled by microdialysis. Norepinephrine levels in spontaneously hypertensive rats were significantly increased and did not change after exposure to neuropeptide Y, in sharp contrast to the decreases seen in Wistar-Kyoto controls. To ascertain whether these alterations in norepinephrine control were specific to the model used, a similar series of experiments was carried out in the paraventricular nucleus of aortic-banded rats. These studies supported the previous findings. Norepinephrine levels in aortic-banded rats were markedly elevated when compared with sham-operated controls and demonstrated no change after exposure to neuropeptide Y, whereas decreases of > 50% were seen in sham-operated controls. These results support the view that mechanisms normally involving neuropeptide Y as a neuromodulator in the paraventricular nucleus are altered in hypertensive situations. It is suggested that hypertension may precipitate changes in mechanisms involving brain neuropeptide Y and increased sympathetic activity.

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