Preferencje help
Polish version English version Język
Widoczny [Schowaj] Abstrakt
Liczba wyników

Znaleziono wyników: 7

Liczba wyników na stronie
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 1 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników

Wyniki wyszukiwania

Wyszukiwano:
w słowach kluczowych:  renal medulla
help Sortuj według:

help Ogranicz wyniki do:
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 1 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników
1

Binding of cadmium in the renal medulla of humans not exposed occupationally to cadmium

100%
Orlowski C., Piotrowski J. K., Swiercz R.
Acta Poloniae Toxicologica
|
1995
|
tom 03
|
nr 2
2
Content available remote

Intrarenal vasodilator systems: NO, prostaglandins and bradykinin. An integrative approach

72%
Sadowski J., Badzynska B.
Journal of Physiology and Pharmacology. Supplement
|
2008
|
tom 59
|
nr 9
105-119
3
Content available remote

Renal tissue NO and intrarenal haemodynamics during experimental variations of NO content in anaesthetised rats

72%
Grzelec-Mojzesowicz M., Sadowski J.
Journal of Physiology and Pharmacology
|
2007
|
tom 58
|
nr 1
Direct renal nitric oxide (NO) measurements were infrequent and no simultaneous measurements of renal cortical and medullary NO and local perfusion were reported. Large-surface NO electrodes were placed in renal cortex and medulla of anaesthetised rats; simultaneously, renal blood flow (RBF, index of cortical perfusion) and medullary laser-Doppler flux (MBF) were determined. NO synthase inhibitors: nonselective (L-NAME) or selective for neuronal NOS (nNOS) (S-methyl-thiocitrulline, SMTC), and NO donor (SNAP), were used to manipulate tissue NO. Baseline tissue NO was significantly higher in medulla (703±49 nM) than in cortex (231±17 nM). Minimal cortical and medullary NO current measured after maximal L-NAME dose (2.4 mg kg-1 i.v.) was taken as tissue NO zero level. This dose decreased RBF and MBF significantly (-43%). SMTC, 1.2 mg kg-1 h-1 i.v., significantly decreased tissue NO by 105±32 nM in cortex and 546±64 nM in medulla, RBF and MBF decreased 30% and 20%, respectively. Renal artery infusion of SNAP, 0.24 mg kg-1 min-1 significantly increased tissue NO by 139±18 nM in cortex and 948±110 nM in medulla. Since inhibition of nNOS decreased medullary NO by 80% and MBF by 20% only, this isoform has probably minor role in the maintenance of medullary perfusion.
4
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
Content available

Biphasic effect of protein kinase C on rat renal cortical Na plus , K plus -ATPase

72%
Beltowski J., Gorny D., Marciniak A.
Journal of Physiology and Pharmacology
|
1998
|
tom 49
|
nr 4
5
Content available remote

Upregulation of angiotensin AT1a receptors mRNA in the heart and renal medulla after myocardial infarction in rats

72%
Milik E., Szczepanska-Sadowska E., Cudnoch-Jedrzejewska A., Dobruch J., Morton M., Koperski L.
Journal of Physiology and Pharmacology
|
2006
|
tom 57
|
nr 3
The myocardial infarct causes prolonged activation of the renin-angiotensin system and profoundly influences cardiac performance and renal excretory capabilities. The aim of the present study was to determine whether the myocardial infarct is also associated with an altered expression of AT1a receptors (AT1aR) mRNA in the heart and the kidney. To this end male Sprague-Dawley rats were subjected either to the left coronary artery ligation or to the sham surgery. Four weeks after the surgery the animals were sacrificed. In 11 infarcted and 10 sham-operated rats expression of AT1aR mRNA in the walls of the left and right ventricle of the heart, and in the renal cortex and renal medulla was determined by semiquantitative PCR method. In another group of 10 infarcted and 14 sham-operated rats the diameter of cardiomyocytes in the left and right cardiac ventricle was determined. The size of the infarct in the rats used for mRNA determination and for morphometric measurements was equal to 29.4 ± 1.8% and to 31.0 ± 1.2 % of the left ventricular wall, respectively. Expression of AT1aR mRNA was significantly greater in the left (P< 0.01) and right ventricle (P<0.03) of the heart in the infarcted than in the sham operated rats. AT1aR mRNA expression was also significantly greater (P<0.02) in the renal medulla of the infarcted rats than in the renal medulla of the sham operated rats whereas no significant difference was found in the renal cortex. The myocardial infarct was associated with a significant increase of diameter of cardiomyocytes of the left ventricle of the heart (P < 0.0001), however there was no significant correlation between changes in AT1aR mRNA expression and diameter of cardiomyocytes. The results provide evidence that the myocardial infarct results in significant and prolonged upregulation of AT1a receptors mRNA expression in the heart and in the medullary region of the kidney.
6
Content available remote

Specific features and roles of renal circulation: angiotensin II revisited

58%
Sadowski J., Badzynska B.
Journal of Physiology and Pharmacology. Supplement
|
2006
|
tom 57
|
nr 11
169-178
The status of intrarenal circulation determines in part renal excretion, affects body fluid homeostasis and has a role in long term control of arterial blood pressure. The vascular resistance in the renal cortex and medulla is determined by interaction of a vast array of vasoactive hormones and paracrine factors; among these the role of constrictor angiotensin II and dilator prostaglandins and nitric oxide may appear to be dominating. The focus of this review and underlying studies is on the mechanisms whereby the microcirculation of the renal medulla is protected against the vasoconstrictor action of angiotensin II. In anaesthetized normal rats the three mentioned active agents or their inhibitors were applied and total renal blood flow and cortical, outer- and inner medullary laser-Doppler fluxes were determined; in some studies renal tissue nitric oxide was measured using selective electrodes. We conclude that angiotensin II, acting via AT1 receptors, constricts the renal cortical vasculature; in the medulla its action is effectively buffered by prostaglandin E2 but most probably not by nitric oxide.
7
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
Content available

The mechanism of Naplus, Kplus -ATPase inhibition by atrial natriuretic factor in rat renal medulla

58%
Beltowski J., Gorny D., Marciniak A.
Journal of Physiology and Pharmacology
|
1998
|
tom 49
|
nr 2
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 1 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników
JavaScript jest wyłączony w Twojej przeglądarce internetowej. Włącz go, a następnie odśwież stronę, aby móc w pełni z niej korzystać.