-transparent.png){kind=logo}
The modulatory effect of Ca on [Arg8]vasopressin-dependent (AVP) cAMP metabolism was studied in medullary collecting tubules (MCT) and medullary ascending limbs (MAL) microdissected from rat kidney. In MCT segments incubated in vitro with AVP, the accumulation of cAMP was enhanced (delta +59%) when Ca was omitted from the incubation medium compared with a medium with 2 mM of ionized calcium (Ca2+). Ionophore A23187 caused a decrease in AVP-stimulated cAMP accumulation in MCT in the presence of 2 mM Ca2+ but not in a Ca2+-free medium. Diltiazem and verapamil enhanced the AVP-stimulated cAMP accumulation in MCT; PTH had no detectable effect. A23187 caused a dose-dependent inhibition of cAMP accumulation stimulated by AVP with forskolin in both MCT and in MAL. However, in MAL the A23187 concentration needed for half-maximum inhibition (6.3 X 10(-6) M) was higher than for MCT (3.9 X 10(-7) M). The maximum inhibition in MAL (-65%) was less than in MCT (-97%). In the presence of 3-isobutyl-1-methylxanthine, AVP-stimulated cAMP accumulation was inhibited by A23187 in MCT (-45%) but not in MAL. Naproxen or ibuprofen did not relieve the inhibitory action of A23187 in MCT. Added Ca2+ inhibited the AVP-stimulated adenylate cyclase in MCT and MAL (half-maximum approximately equal to 5 X 10(-4) M Ca2+) and stimulated cAMP phosphodiesterase (cAMP-PDIE) in both MCT and in MAL (half-maximum approximately equal to 9 X 10(-5) M Ca2+). Incubation of MCT and MAL with A23187 decreased (-50%) the content of ATP. Results suggest that increased influx of extracellular Ca2+ inhibits the AVP-stimulated cAMP accumulation in MCT and to a much lesser degree in MAL. Deceased cAMP accumulation in MCT is probably due to both stimulation of cAMP-PDIE and the inhibition of adenylate cyclase, whereas in MAL it is due to stimulation of cAMP-PDIE. The results suggest that Ca2+ influx exhibits a negative modulatory effect on AVP-dependent cAMP metabolism mainly in MCT.
E Kusano, and
N Murayama, and
J L Werness, and
S Christensen, and
S Homma, and
A N Yusufi, and
T P Dousa
January 1982,
The Journal of laboratory and clinical medicine,
E Kusano, and
N Murayama, and
J L Werness, and
S Christensen, and
S Homma, and
A N Yusufi, and
T P Dousa
June 1988,
Molecular and cellular endocrinology,
E Kusano, and
N Murayama, and
J L Werness, and
S Christensen, and
S Homma, and
A N Yusufi, and
T P Dousa
September 1994,
The American journal of physiology,
E Kusano, and
N Murayama, and
J L Werness, and
S Christensen, and
S Homma, and
A N Yusufi, and
T P Dousa
January 1992,
Pharmacology,
E Kusano, and
N Murayama, and
J L Werness, and
S Christensen, and
S Homma, and
A N Yusufi, and
T P Dousa
June 1987,
The American journal of physiology,
E Kusano, and
N Murayama, and
J L Werness, and
S Christensen, and
S Homma, and
A N Yusufi, and
T P Dousa
January 1994,
Renal physiology and biochemistry,
E Kusano, and
N Murayama, and
J L Werness, and
S Christensen, and
S Homma, and
A N Yusufi, and
T P Dousa
March 1972,
The American journal of physiology,
E Kusano, and
N Murayama, and
J L Werness, and
S Christensen, and
S Homma, and
A N Yusufi, and
T P Dousa
August 1988,
The American journal of physiology,
E Kusano, and
N Murayama, and
J L Werness, and
S Christensen, and
S Homma, and
A N Yusufi, and
T P Dousa
August 2005,
Hypertension research : official journal of the Japanese Society of Hypertension,
E Kusano, and
N Murayama, and
J L Werness, and
S Christensen, and
S Homma, and
A N Yusufi, and
T P Dousa
July 1993,
The American journal of physiology,
