scholarly journals RENIN SECRETION IN THE PERFUSED DOG KIDNEY

1968 ◽  
Vol 18 (1) ◽  
pp. 1-8 ◽  
Author(s):  
KENJIRO YAMAMOTO ◽  
TAKAMICHI HASEGAWA ◽  
JURO UEDA
Keyword(s):  
Author(s):  
Gunter F. Thomas ◽  
M. David Hoggan

In 1968, Sugimura and Yanagawa described a small 25 nm virus like particle in association with the Matsuda strain of infectious canine hepatitis virus (ICHV). Domoto and Yanagawa showed that this particle was dependent on ICHV for its replication in primary dog kidney cell cultures (PDK) and was resistant to heating at 70°C for 10 min, and concluded that it was a canine adeno-associated virus (CAAV). Later studies by Onuma and Yanagawa compared CAAV with the known human serotypes (AAV 1, 2, 3) and AAV-4, known to be associated with African Green Monkeys. Using the complement fixation (CF) test, they found that CAAV was serologically related to AAV-3 and had wide distribution in the dog population of Japan.


Author(s):  
J. A. Nowell ◽  
J. Pangborn ◽  
W. S. Tyler

Leonardo da Vinci in the 16th century, used injection replica techniques to study internal surfaces of the cerebral ventricles. Developments in replicating media have made it possible for modern morphologists to examine injection replicas of lung and kidney with the scanning electron microscope (SEM). Deeply concave surfaces and interrelationships to tubular structures are difficult to examine with the SEM. Injection replicas convert concavities to convexities and tubes to rods, overcoming these difficulties.Batson's plastic was injected into the renal artery of a horse kidney. Latex was injected into the pulmonary artery and cementex in the trachea of a cat. Following polymerization the tissues were removed by digestion in concentrated HCl. Slices of dog kidney were aldehyde fixed by immersion. Rat lung was aldehyde fixed by perfusion via the trachea at 30 cm H2O. Pieces of tissue 10 x 10 x 2 mm were critical point dried using CO2. Selected areas of replicas and tissues were coated with silver and gold and examined with the SEM.


2014 ◽  
Vol 8 (1) ◽  
pp. 32-38
Author(s):  
Amani Abbas ◽  
Hemmat Alemam ◽  
Hanan El-zawahry

Hypertension ◽  
1995 ◽  
Vol 26 (1) ◽  
pp. 137-142 ◽  
Author(s):  
Xiao-Rui He ◽  
Suzanne G. Greenberg ◽  
Josie P. Briggs ◽  
Jürgen Schnermann
Keyword(s):  

1988 ◽  
Vol 255 (5) ◽  
pp. R794-R798 ◽  
Author(s):  
N. M. Rawashdeh ◽  
J. C. Rose ◽  
N. D. Ray

To study the functional maturity of beta-receptor-mediated responses, seven chronically catheterized lamb fetuses, 93-107 days of gestation, and seven fetuses, 116-134 days of gestation, received intravenous randomly sequenced infusions of isoproterenol (ISO) 0.03, 0.06, and 0.125 micrograms.kg-1.min-1 for 10 min separated by 45-min intervals or two saline infusions followed by 0.125 micrograms.kg-1.min-1 ISO after treatment with 0.5 mg/kg propranolol (PRO). Each fetus received the two treatments 24-48 h apart. In immature fetuses, plasma renin activity (PRA) of 2.0 +/- 0.7 ng.ml-1.h-1 did not change with either protocol. In mature fetuses, PRA of 7.5 +/- 2.5 ng.ml-1.h-1 increased two- to three-fold after the infusion of the highest two doses of ISO (P less than 0.003). Propranolol blocked this response. No significant changes were observed after the infusions of the lowest dose of ISO or saline. Both groups showed significant heart rate increases with all doses of ISO. Propranolol injection decreased heart rate significantly and blocked responses to ISO. We conclude that although a cardiac beta-receptor-mediated response is present by 93 days of gestation in the lamb fetus, a renal beta-receptor-mediated response, renin secretion, is absent.


1989 ◽  
Vol 257 (4) ◽  
pp. R765-R770 ◽  
Author(s):  
K. T. Nakamura ◽  
J. M. Klinkefus ◽  
F. G. Smith ◽  
T. Sato ◽  
J. E. Robillard

The role of renal nerves and norepinephrine release on renin secretion during fetal and postnatal maturation has not been studied. Experiments were performed to determine the effect of veratridine, a substance known to promote norepinephrine release from nerve terminals, on active and inactive renin secretion from renal cortical slices of fetal (134-138 days gestation; term is 145 days), newborn (4-9 days of age), and adult nonpregnant sheep. Veratridine (10-300 microM) significantly increased active renin secretion and produced a small but nonsignificant rise in inactive renin secretion in all three groups of animals (P less than 0.05). The percent rise in active renin secretion during veratridine stimulation was similar among all groups. Veratridine-stimulated (300 microM) active renin secretion was antagonized by tetrodotoxin (0.5 and 5.0 microM) and DL-propranolol (1 microM) in fetal renal cortical slices. However, neither tetrodotoxin nor propranolol completely inhibited the stimulatory effect of veratridine on active renin secretion. These results suggest that 1) norepinephrine released from nerve terminals may regulate active renin secretion early during development; 2) the effect of veratridine on active renin secretion was similar in fetal, newborn, and adult sheep; 3) veratridine had no significant effect on inactive renin secretion; and 4) active renin secretion due to depolarization of nerve terminals in fetal sheep is dependent on activation of beta-adrenoceptors as it is in adults.


1995 ◽  
Vol 269 (1) ◽  
pp. F134-F139 ◽  
Author(s):  
W. H. Beierwaltes

The macula densa is a regulatory site for renin. It contains exclusively the neuronal isoform of nitric oxide synthase (NOS), suggesting NO could stimulate renin secretion through the macula densa pathway. To test whether neuronal NOS mediates renin secretion, renin was stimulated by either the renal baroreceptor or the diuretic furosemide (acting through the macula densa pathway). Renin secretion rate (RSR) was measured in 12 Inactin-anesthetized rats at normal (104 +/- 3 mmHg) and reduced renal perfusion pressure (65 +/- 1 mmHg), before and after selective blockade of the neuronal NOS with 7-nitroindazole (7-NI, 50 mg/kg ip). 7-NI had no effect on basal blood pressure (102 +/- 2 mmHg) or renal blood flow (RBF). Decreasing renal perfusion pressure doubled RSR from 11.8 +/- 3.3 to 22.9 +/- 5.7 ng ANG I.h-1.min-1 (P < 0.01) (ANG I is angiotensin I). Similarly, in 7-NI-treated rats, reduced perfusion doubled RSR from 8.5 +/- 1.8 to 20.5 +/- 6.2 ng ANG I.h-1.min-1 (P < 0.01). Renal hemodynamics and RSR were measured in response to 5 mg/kg iv furosemide in 12 control rats and 11 rats treated with 7-NI. Blocking neuronal NOS did not alter blood pressure (102 +/- 2 mmHg), RBF (5.8 +/- 0.4 ml.min-1.g kidney wt-1), or renal vascular resistance (18.7 +/- 1.4 mmHg.ml-1.min.g kidney wt).(ABSTRACT TRUNCATED AT 250 WORDS)


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