Voiding behavior in awake unrestrained untethered spontaneously hypertensive and Wistar control rats

2021 ◽  
Author(s):  
Christopher L Langdale ◽  
Danielle J Degoski ◽  
Philip H Milliken ◽  
Warren M. Grill
Keyword(s):  
Body Weight ◽  
Water Consumption ◽  
Genetic Model ◽  
Spontaneously Hypertensive Rat ◽  
Infusion Pump ◽  
Bladder Capacity ◽  
In Vivo Studies ◽  
Spontaneously Hypertensive ◽  
Voided Volume

The spontaneously hypertensive rat (SHR), a genetic model of high blood pressure, has also been studied as a potential model of overactive bladder (OAB). In vivo studies confirmed the presence of surrogate markers of OAB, including detrusor overactivity (DO), increased urinary frequency, decreased bladder capacity and voided volume, and afferent hypersensitivity to bladder irritation. However, these observations were during awake cystometry (CMG) using implanted bladder catheters tethered to an infusion pump and artificially filled. We conducted studies in awake unrestrained untethered age-matched female SHR and Wistar rats to quantify naïve consumption and voiding behavior and the effect of capsaicin desensitization on consumption and voiding behavior. Food and water consumption, body weight, voiding frequency (VF), and voided volume (VV) were recorded. Rats were placed in metabolism cages for 24 h, up to twice a week, from 17 to 37 weeks of age. In SHRs, body weight, food, and water consumption were decreased compared to Wistars. However, after normalizing for body weight, only water consumption was reduced. Wistars exhibited a diurnal pattern of voiding behavior. Compared to Wistars, SHRs showed smaller VV and lacked a diurnal voiding pattern such that VV was similar during both light cycles. No difference in VF was observed after normalizing for water consumption. We observed no change in SHR voiding behavior following capsaicin desensitization, which was in contrast to a prior awake in vivo cystometry study describing increased VV and micturition interval in SHRs, and suggests that C-fiber activity may not contribute to bladder hypersensitivity in SHRs.

scholarly journals Effective Control of Postprandial Glucose Level through Inhibition of Intestinal Alpha Glucosidase byCymbopogon martinii(Roxb.)

2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Varsha Ghadyale ◽  
Shrihari Takalikar ◽  
Vivek Haldavnekar ◽  
Akalpita Arvindekar
Keyword(s):  
Body Weight ◽  
Silica Gel ◽  
Glucose Level ◽  
Postprandial Glucose ◽  
Hot Water ◽  
In Vivo Studies ◽  
Effective Control ◽  
Alpha Glucosidase ◽  
Postprandial Glucose Level

Inhibition of intestinal alpha glucosidase plays a major role in preventing rise in postprandial glucose level in diabetics.Cymbopogon martinii(CM) (family Poaceae) is used in traditional Indian medicine in treatment of diabetes mellitus. The alpha glucosidase inhibitory action of the plant is studied. The active component was separated using hot water extraction of the whole plant powder, differential solvent extraction, and silica gel column chromatography. The 30 : 70 toluene : ethyl acetate fraction showed optimum activity. The silica gel chromatography fraction demonstrated 98, 98, and 68% inhibition for starch, maltose, and sucrose, respectively, at 5 mg/kg body weight of rats. Intestinal absorption studies using noneverted intestinal sacs, as well as in vivo studies in streptozotocin-induced diabetic rats using oral glucose tolerance with maltose and sucrose load, revealed better inhibition of alpha glucosidase as compared to acarbose. Kinetic studies using Lineweaver Burk plot showed mixed to noncompetitive type of inhibition by CM. In vivo studies with maltose load of 2 mg and 3 mg/gm body weight showed a noncompetitive pattern of inhibition at 5 mg/kg body weight of CM as against 60 mg/kg body weight of acarbose. Thus CM is more effective alpha glucosidase inhibitor and at lower concentration than acarbose.

Role of adenosine in noradrenergic neurotransmission in spontaneously hypertensive rats

1987 ◽  
Vol 253 (4) ◽  
pp. H909-H918 ◽  
Author(s):  
E. K. Jackson
Keyword(s):  
Plasma Levels ◽  
Spontaneously Hypertensive Rat ◽  
Base Line ◽  
Inhibitory Effects ◽  
Spontaneously Hypertensive ◽  
Vascular Responses ◽  
Rat Mesentery ◽  
Wistar Kyoto

The purpose of this study was to compare the in vivo role of adenosine as a modulator of noradrenergic neurotransmission in the spontaneously hypertensive rat (SHR) and Wistar-Kyoto control rat (WKY). In the in situ blood-perfused rat mesentery, vascular responses to periarterial (sympathetic) nerve stimulation (PNS) and to exogenous norepinephrine (NE) were enhanced in SHR compared with WKY. In both SHR and WKY, vascular responses to PNS were more sensitive to inhibition by adenosine than were responses to NE. At matched base-line vascular responses, compared with WKY, SHR were less sensitive to the inhibitory effects of adenosine on vascular responses to PNS, but SHR and WKY were equally sensitive with respect to adenosine-induced inhibition of responses to NE. Antagonism of adenosine receptors with 1,3-dipropyl-8-p-sulfophenylxanthine shifted the dose-response curve to exogenous adenosine sixfold to the right yet did not influence vascular responses to PNS or NE in either SHR or WKY. Furthermore, PNS did not alter either arterial or mesenteric venous plasma levels of adenosine in SHR or WKY, and plasma levels of adenosine in both strains were always lower than the calculated threshold level required to attenuate neurotransmission. It is concluded that in vivo 1) exogenous adenosine interferes with noradrenergic neurotransmission in both SHR and WKY; 2) SHR are less sensitive to the inhibitory effects of exogenous adenosine on noradrenergic neurotransmission than are WKY; 3) endogenous adenosine does not play a role in modulating neurotransmission in either strain under the conditions of this study; and 4) enhanced noradrenergic neurotransmission in the SHR is not due to defective modulation of neurotransmission by adenosine.

Nerve Growth Factor Enhances Calcitonin Gene-Related Peptide Expression in the Spontaneously Hypertensive Rat

Hypertension ◽  
2000 ◽  
Vol 36 (suppl_1) ◽  
pp. 701-701
Author(s):  
M Huawei Zhao ◽  
M Scott C Supowit ◽  
M Donald J DiPette
Keyword(s):  
Spontaneously Hypertensive Rat ◽  
Day Treatment ◽  
Fold Increase ◽  
Spontaneously Hypertensive ◽  
Treatment Groups ◽  
Continuous Map ◽  
Potent Vasodilator ◽  
Peptide Expression ◽  
Cgrp Receptor Antagonist

P45 We previously reported that there is a marked decrease in neuronal (dorsal root ganglia [DRG] sensory neurons) CGRP expression in the SHR compared to WKY controls. This reduction in such a potent vasodilator could contribute to the elevated BP. We hypothesize that administration of NGF, a potent in vivo stimulator of CGRP expression, to SHR would decrease the BP. NGF (10 nM/kg/day, i.p.) was given to 12 week SHR (n=8-11/group) once a day for 1, 3, and 7 days. Control SHR received vehicle only. All rats were instrumented for CGRP receptor antagonist (CGRP 8-37 ) administration (i.v.) and continuous MAP (arterial) recording and were studied in a concious and unrestrained state. Both the 1 and 3 day NGF treatments lowered the MAP (147±5 and 147±3 mmHg; respectively, p<0.05) compared to the controls (166±3 mmHg). However, by day 7 the MAP had returned to control levels (169±5 mmHg). To determine whether CGRP was involved in the BP lowering response to NGF, saline or CGRP 8-37 (bolus dose of 200 μg) were administered i.v. to all rats. Saline was without effect in any of the groups studied. In contrast, CGRP 8-37 administration produced a significant increase in MAP in both the 1 (13±1 mmHg) and 3 (10±1 mmHg) day NGF treatment groups. Surprisingly, in the 7 day treatment group, CGRP 8-37 also increased the MAP (13±2 mmHg) despite the baseline BP being back up to control levels. Quantification of CGRP mRNA and peptide levels in DRG revealed a significant (p<0.05) 1.5-fold increase on days 1 and 3 and a 1.75-fold increase on day 7. These data demonstrate that NGF treatment of SHR can significantly increase neuronal CGRP expression. At days 1 and 3, NGF produces a marked depressor response that is primarily due to CGRP as evidenced by the pressor effect of CGRP 8-37 . In the day 7 group, CGRP also plays a counterregulatory role even though the MAP has returned to control levels. This may result from an NGF-mediated upregulation of a pressor system that counteracts the hypotensive actions of CGRP. These results, therefore, suggest that the decreased production of CGRP in the SHR could contribute to the elevated BP observed in this hypertensive model.

Analysis of BP response and Ca2+ metabolism using the saturation kinetics model

1987 ◽  
Vol 253 (3) ◽  
pp. R501-R508
Author(s):  
N. Karanja ◽  
J. A. Metz ◽  
L. P. Mercer ◽  
D. A. McCarron
Keyword(s):  
Blood Pressure ◽  
Body Weight ◽  
Bone Density ◽  
Spontaneously Hypertensive Rat ◽  
Kinetics Model ◽  
Maximal Dose ◽  
Spontaneously Hypertensive ◽  
Rates Of Change ◽  
Saturation Kinetics ◽  
Serum Ionized Calcium

The provision of supplemental dietary calcium (dCa) lowers blood pressure (BP) in the spontaneously hypertensive rat (SHR). Whether calcium's antihypertensive effects can be expressed in the presence of potentially hypertensinogenic nutrients is not known. Furthermore, the amount of dCa required to attenuate hypertension in the SHR remains undetermined. Along with establishing the effects of dCa on BP under conditions of a high Na+ intake, we sought to define the lowest dose of dCa associated with the greatest attenuation in arterial pressure in the young SHR. Thirty-five 6-wk-old SHR were fed one of five diets containing either 0.1, 0.25, 0.5, 1.0, or 2.0% dCa. All diets contained 1.0% Na+. The rates of change (delta) in body weight, BP, and serum ionized calcium were determined between 6 and 20 wk of age. Bone density (BD) was measured only at 20 wk of age. The data were analyzed using the saturation kinetics model. Results indicate that the half-maximal dose (K50) of dCa needed to lower pressure is 0.67 +/- 0.18%, which is higher than the K50 for weight (0.23 +/- 0.18) and BD (0.36 +/- 0.22). It is concluded that supplemental dCa lowers BP despite a high Na+ intake. Furthermore, a dose of approximately 1.5 dCa is sufficient to attenuate the rate of hypertension in the young growing SHR.

Pathogenesis of abnormal acid–base balance in the young spontaneously hypertensive rat

1988 ◽  
Vol 75 (1) ◽  
pp. 29-34 ◽  
Author(s):  
Philip A. Lucas ◽  
Bernard Lacour ◽  
Lydie Comte ◽  
Tilman Drüeke
Keyword(s):  
Body Weight ◽  
Spontaneously Hypertensive Rat ◽  
Intraperitoneal Administration ◽  
Urinary Sodium ◽  
Ammonium Ion ◽  
Spontaneously Hypertensive ◽  
Plasma Bicarbonate ◽  
Phosphate Excretion ◽  
Blood Ph ◽  
Acid Loading

1. We have previously reported reduced blood pH and plasma bicarbonate in young Okamoto–Aoki spontaneously hypertensive rats (SHR) compared with normotensive Wistar–Kyoto rats (WKY). Acid loading with 1.5% (w/v) NH4Cl as the sole drinking fluid produced identical falls in blood pH, the difference remaining significant. 2. The ability of SHR to excrete acid and alkaline loads was compared with that of WKY under metabolic cage conditions. The effects of such manipulations on urinary sodium, potassium, calcium and phosphate excretion were also determined. 3. No difference was found in the ability to excrete an acid load or to reduce urine pH. Neither total urinary ammonium ion nor titratable acid differed significantly between the strains under either baseline or acid-loading conditions. 4. Baseline urinary bicarbonate excretion was not significantly different between strains but intraperitoneal administration of NaHCO3 at 2.0 mmol/kg body weight resulted in enhanced excretion in the SHR (SHR vs WKY: 625.2±71.5 vs 381.8±40.6 μmol 24h−1 kg−1 body weight, P < 0.01, mean±sem). 5. No difference in urinary sodium or potassium excretion was observed between SHR and WKY, but basal calcium and phosphate excretion were reduced in SHR (P < 0.05). 6. Increased urinary bicarbonate excretion in the presence of significantly reduced plasma bicarbonate suggests reduced tubular reabsorption of bicarbonate, which may contribute to the mild metabolic acidosis in young SHR.

Development of a Full Flexion 3D Musculoskeletal Model of the Knee Considering Intersegmental Contact During High Knee Flexion Movements

2020 ◽  
Vol 36 (6) ◽  
pp. 444-456
Author(s):  
David C. Kingston ◽  
Stacey M. Acker
Keyword(s):  
Body Weight ◽  
Knee Flexion ◽  
Knee Extensor ◽  
Musculoskeletal Model ◽  
Contact Forces ◽  
Model Verification ◽  
In Vivo Studies ◽  
Muscle Groups ◽  
The Right

A musculoskeletal model of the right lower limb was developed to estimate 3D tibial contact forces in high knee flexion postures. This model determined the effect of intersegmental contact between thigh–calf and heel–gluteal structures on tibial contact forces. This model includes direct tracking and 3D orientation of intersegmental contact force, femoral translations from in vivo studies, wrapping of knee extensor musculature, and a novel optimization constraint for multielement muscle groups. Model verification consisted of calculating the error between estimated tibial compressive forces and direct measurements from the Grand Knee Challenge during movements to ∼120° of knee flexion as no high knee flexion data are available. Tibial compression estimates strongly fit implant data during walking (R2 = .83) and squatting (R2 = .93) with a root mean squared difference of .47 and .16 body weight, respectively. Incorporating intersegmental contact significantly reduced model estimates of peak tibial anterior–posterior shear and increased peak medial–lateral shear during the static phase of high knee flexion movements by an average of .33 and .07 body weight, respectively. This model supports prior work in that intersegmental contact is a critical parameter when estimating tibial contact forces in high knee flexion movements across a range of culturally and occupationally relevant postures.

Intestinal calcium transport in the spontaneously hypertensive rat: response to calcium depletion

1986 ◽  
Vol 250 (4) ◽  
pp. G412-G419
Author(s):  
H. P. Schedl ◽  
D. L. Miller ◽  
R. L. Horst ◽  
H. D. Wilson ◽  
K. Natarajan ◽  
...  
Keyword(s):  
Vitamin D ◽  
Small Intestine ◽  
Calcium Transport ◽  
Spontaneously Hypertensive Rat ◽  
Calcium Depletion ◽  
Spontaneously Hypertensive ◽  
Distal Small Intestine ◽  
Wistar Kyoto

We previously found intestinal Ca2+ transport to be lower in the spontaneously hypertensive (SH) as compared with the Wistar-Kyoto control (WKY) rat. These animals were fed a relatively high (1%) Ca2+ diet, and the concentration of 1 alpha,25-dihydroxycholecalciferol [1 alpha,25(OH)2D3] in serum was the same in both groups. In the present experiment we tested the possibility that the lower Ca2+ transport in the SH rat was the result of unresponsiveness to 1 alpha,25(OH)2D3. We fed diets high and low in Ca2+ and measured serum 1 alpha,25(OH)2D3 and Ca2+ transport. Serum 1 alpha,25(OH)2D3 increased in response to Ca2+ depletion at both 5 and 12 wk in both the WKY and SH rat. With high-Ca2+ diet, Ca2+ transport was lower in SH than in WKY when studied 1) in vitro in duodenum at 5 wk of age, and 2) in vivo in proximal and distal small intestine at 12 wk of age. Ca2+ transport increased in SH in response to Ca2+ depletion, but not in WKY, except in distal small intestine in vivo at 12 wk. In summary, although Ca2+ transport is lower in the SH as compared with the WKY rat when vitamin D activity is basal through feeding a high-Ca2+ diet, Ca2+ transport increases in the SH rat in response to the increase in 1 alpha,25(OH)2D3 produced by feeding a low-Ca2+ diet. We conclude that 1) the vitamin D-regulated component of mediated Ca2+ transport is intact in the SH rat and is unrelated to hypertension, and 2) mediated Ca2+ transport under basal conditions, i.e., nonvitamin D-regulated, differs in the SH and WKY rats and may be related to hypertension.

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