Intravital microscopical studies of the tubular urine flow in the conscious rat

1. The urinary excretion of prostaglandin E2 (PGE2) was measured in conscious rats under conditions which produced either acid or alkaline urine, but similar change in fluid and solute excretion. 2. Oral isotonic saline increased both urine flow and sodium excretion but did not alter urinary PGE2 output (which remained constant at 80 pmol/3 h per rat) or urine pH (6.2). 3. When the urine was made alkaline (pH 7.8) by oral sodium bicarbonate or carbonate, urinary PGE2 was approximately 3-fold greater (P<0.00l) than the control (pH6.2). The urine flow and sodium output were also increased. 4. When the urine was made acidic (pH 5.7) by oral ammonium chloride, urinary PGE, excretion was reduced (P<0.01) to approximately half the control output. The urine flow and sodium output increased. 5. Within a group of 12 rats receiving oral isotonic saline a positive linear correlation coefficient (P<0.002) was established between urine pH and PGE2 excretion. 6. The results indicate that urine pH may be a determinant of PGE2 excretion in unrestrained, conscious rats. It seems likely that this effect of pH is mediated by a change in the passive reabsorption of PGE, in the distal nephron, although alternative explanations such as altered tubular secretion or synthesis cannot be categorically excluded.

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Renal effects of acute endothelial-derived relaxing factor blockade are not mediated by angiotensin II

AJP Renal Physiology ◽

10.1152/ajprenal.1993.264.1.f74 ◽

1993 ◽

Vol 264 (1) ◽

pp. F74-F78 ◽

Cited By ~ 9

Author(s):

C. Baylis ◽

K. Engels ◽

L. Samsell ◽

P. Harton

Keyword(s):

Angiotensin Ii ◽

Sodium Excretion ◽

Renal Plasma Flow ◽

Urine Flow ◽

Sodium Reabsorption ◽

Ang Ii ◽

Conscious Rat ◽

Relaxing Factor ◽

Renal Hemodynamic ◽

Renal Vascular

The renal responses to acute blockade of the endothelial-derived relaxing factor (EDRF) resemble the renal actions of angiotensin II (ANG II), and the present studies were conducted to establish what role, if any, the endogenous renin-angiotensin system plays in mediating the renal response to acute EDRF blockade. These studies were conducted in the conscious chronically catheterized rat. In control experiments we observed that acute blockade of ANG II synthesis with converting-enzyme inhibition (CEI) led to a fall in blood pressure (BP) and a slight renal vasodilation but no significant change in glomerular filtration rate (GFR) or renal plasma flow (RPF). Urine flow and sodium excretion were unchanged by CEI. Use of the nonpeptide ANG II receptor antagonist losartan had no effect on BP, renal vascular resistance (RVR), GFR, or RPF; however, urine flow and sodium excretion did rise significantly. Because of the high specificity of losartan, this suggests that, in the normal conscious rat, endogenous ANG II does not control renal vascular tone but does enhance renal sodium reabsorption. ANG II blockade with either CEI or losartan had little effect on BP and no effect on the renal hemodynamic responses to acute EDRF blockade. The marked natriuretic and diuretic response to acute EDRF blockade persists during concomitant losartan but is abolished by CEI. These studies suggest that in the conscious rat the renal hemodynamic response to EDRF blockade is not mediated by endogenous ANG II.

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Dual modulation of urinary bladder activity and urine flow by prostanoid EP3receptors in the conscious rat

British Journal of Pharmacology ◽

10.1111/j.1476-5381.2009.00275.x ◽

2009 ◽

Vol 158 (1) ◽

pp. 372-381 ◽

Cited By ~ 21

Author(s):

MJ Jugus ◽

JP Jaworski ◽

PB Patra ◽

J Jin ◽

DM Morrow ◽

...

Keyword(s):

Urinary Bladder ◽

Urine Flow ◽

Conscious Rat ◽

Bladder Activity

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Antidiuretic effect of acute morphine administration in the conscious rat

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y82-031 ◽

1982 ◽

Vol 60 (2) ◽

pp. 201-204 ◽

Cited By ~ 12

Author(s):

N. Wilson ◽

J. Ngsee

Keyword(s):

Mean Arterial Pressure ◽

Arterial Pressure ◽

Diabetes Insipidus ◽

Antidiuretic Hormone ◽

Urine Flow ◽

Conscious Rat ◽

Antidiuretic Effect ◽

Morphine Administration

Morphine was administered intravenously to normal and to Brattleboro (genetically deficient in antidiuretic hormone) rats. The injection caused a significant decrease in mean arterial pressure and urine flow in all animals, including those homozygous for diabetes insipidus. It is suggested that the antidiuretic effect of morphine may occur independently of ADH release.

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EFFECTS OF ARGININE-, LYSINE- AND LEUCINE-VASOPRESSIN ON URINARY OSMOLALITY AND RATE OF URINE FLOW IN HYDRATED RATS AND DOGS

Acta Endocrinologica ◽

10.1530/acta.0.xxxii0134 ◽

1959 ◽

Vol XXXII (I) ◽

pp. 134-141 ◽

Cited By ~ 10

Author(s):

Niels A. Thorn

Keyword(s):

Arginine Vasopressin ◽

Urine Osmolality ◽

Urine Flow ◽

The Other ◽

Maximum Increase ◽

Urinary Osmolality ◽

Lysine Vasopressin

ABSTRACT Arginine-, lysine- and leucine-vasopressin, injected i. v. into hydrated rats or dogs caused different patterns of response in that urine osmolality fell much more slowly after the maximum increase following arginine-vasopressin, than after the other two preparations. Using 3 different parameters for antidiuretic response, arginine-vasopressin was somewhat more potent than leucine-vasopressin in both rats and dogs, considerably more potent than lysine-vasopressin in rats, and much more so in dogs.

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Faculty Opinions recommendation of Effects of chronic coffee consumption on glucose kinetics in the conscious rat.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1092349.546771 ◽

2007 ◽

Author(s):

Michael Clark

Keyword(s):

Coffee Consumption ◽

Glucose Kinetics ◽

Conscious Rat

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Role of Uttarabasti in the management of Functional Bladder Outlet Obstruction: A Case Study

Journal of Ayurveda and Integrated Medical Sciences (JAIMS) ◽

10.21760/jaims.v2i3.8243 ◽

2017 ◽

Vol 2 (3) ◽

Author(s):

Jaimin R. Patel

Keyword(s):

Bladder Outlet Obstruction ◽

Outlet Obstruction ◽

Urine Flow ◽

Complete Relief ◽

Urinary Flow ◽

Detrusor Sphincter Dyssynergia ◽

Symptom Appraisal ◽

Prostatic Enlargement ◽

Normal Urine ◽

Outflow Channel

Bladder outlet obstruction (BOO) produces compression or resistance upon the bladder outflow channel at any location from the bladder neck to urethral meatus. It may be induced by specific functional and anatomic causes. Functional obstruction may be caused by detrusor-sphincter dyssynergia (DSD) and anatomic obstruction most commonly from benign prostatic enlargement (BPH) or urethral stricture. Obstructive symptoms include hesitancy, sensation of incomplete bladder emptying, diminished urinary stream. The combination of PVR, urinary flow measures, and symptom appraisal has been generally accepted as the initial screening and evaluation paradigm for BOO. In, Ayurveda, BOO is similar to Mutraghata means obstruction in the urine flow. Uttarbasti is the prime treatment of Mutraghata. Present case is diagnosed as a functional bladder outlet obstruction (BOO) on the basis of symptoms, normal reports of USG and ascending urethrogram and diminished flow of urine in Uroflowmetry. Total 7 Uttarbasti with 50ml Sahcharadi Tailam was given along with Rasayana and Mutraghatahara medicine. Patient has complete relief in his obstructive urine complains and has normal urine flow without taking Tab. AFDURA after 7 years. And also improvement appear in Uroflowmetry.

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