Atrial natriuretic peptide initiates Ca2+ transients in isolated renal cortical thick ascending limb cells

Dai LJ, and Quamme GA: Atrial natriuretic peptide initiates Ca2+ transients in isolated renal  cortical thick ascending limb cells. American Journal of Physiology 265:F592-F597, 1993.

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Abstract Atria1 natriuretic peptide initiates Ca2+ transients in isolated renal cortical thick ascending limb cells. Am. J. Physiol. 265 (Renal Fluid Electrolyte PhysioZ. 34): F592-F597, 1993.-The following studies identified and characterized atria1 natriuretic peptide (ANP) receptor-mediated Ca2+ transients in cortical thick ascending limb (CTAL) cells. Primary cell cultures were prepared from porcine kidneys by immunodissection, and intracellular Ca2+ concentration ([Ca”+]J was determined in single cells with microfluorometry. ANP (10m7M ) and its analogue,C -type natriuretic peptide (CNP, 10m7M ), elicited Ca2+t ransients [ 104 t 6 (basal levels) to 653 & 112 nM (stimulated) and from 84 t 4 to 209 & 18 nM, respectively]. Receptor-mediated [ Ca2+]i increase was dose-dependenwt ith a 50% effective concentration (EC,,) of N lo-lo M. The increment in [Ca”‘]i was due to internal release and influx across the plasma membrane. Prior treatment of ANP or CNP (10q7 M) did not markedly affect a post application of either ANP or CNP. The truncated analogue of ANP, C-ANP-(4-23), which preferentially binds to clearance receptors, elicited an increase in [Ca”+]i (82 & 1 to 427 t 41 nM). 8-Bromoguanosine 3’,5’-cyclic monophosphate (8-BrcGMP) did not alter [Ca”+]i, but pretreatment of CTAL cells with 8-BrcGMP for 30 min before agonist treatment prevented ANP-induced Ca2+ signals [83 t 5 (basal) to 88 t 5 nM (stimulated)]. These results are evidence for the existence of clearance ANP receptors in CTAL cells that may have biological functions and clearance. The functional responseso f these signal interactions may have important consequenceosn hormone actions with the CTAL.

Atria1 natriuretic

peptide initiates Ca2+ transients in isolated renal cortical thick

ascending limb cells. Am. J. Physiol. 265 (Renal Fluid Electrolyte

PhysioZ. 34): F592-F597, 1993.-The following studies

identified and characterized atria1 natriuretic peptide (ANP)

receptor-mediated Ca2+ transients in cortical thick ascending

limb (CTAL) cells. Primary cell cultures were prepared from

porcine kidneys by immunodissection, and intracellular Ca2+

concentration ([Ca”+]J was determined in single cells with microfluorometry.

ANP (10m7M ) and its analogue,C -type natriuretic

peptide (CNP, 10m7M ), elicited Ca2+t ransients [ 104 t 6

(basal levels) to 653 & 112 nM (stimulated) and from 84 t 4 to

209 & 18 nM, respectively]. Receptor-mediated [ Ca2+]i increase

was dose-dependenwt ith a 50% effective concentration (EC,,)

of N lo-lo M. The increment in [Ca”‘]i was due to internal

release and influx across the plasma membrane. Prior treatment

of ANP or CNP (10q7 M) did not markedly affect a post application

of either ANP or CNP. The truncated analogue of ANP,

C-ANP-(4-23), which preferentially binds to clearance receptors,

elicited an increase in [Ca”+]i (82 & 1 to 427 t 41 nM).

8-Bromoguanosine 3’,5’-cyclic monophosphate (8-BrcGMP)

did not alter [Ca”+]i, but pretreatment of CTAL cells with

8-BrcGMP for 30 min before agonist treatment prevented

ANP-induced Ca2+ signals [83 t 5 (basal) to 88 t 5 nM (stimulated)].

These results are evidence for the existence of clearance

ANP receptors in CTAL cells that may have biological functions

and clearance. The functional responseso f these signal

interactions may have important consequenceosn hormone actions

with the CTAL.

porcine thick ascendingAtria1 natriuretic

peptide initiates Ca2+ transients in isolated renal cortical thick
ascending limb cells. Am. J. Physiol. 265 (Renal Fluid Electrolyte
PhysioZ. 34): F592-F597, 1993.-The following studies
identified and characterized atria1 natriuretic peptide (ANP)
receptor-mediated Ca2+ transients in cortical thick ascending
limb (CTAL) cells. Primary cell cultures were prepared from
porcine kidneys by immunodissection, and intracellular Ca2+
concentration ([Ca”+]J was determined in single cells with microfluorometry.
ANP (10m7M ) and its analogue,C -type natriuretic
peptide (CNP, 10m7M ), elicited Ca2+t ransients [ 104 t 6
(basal levels) to 653 & 112 nM (stimulated) and from 84 t 4 to
209 & 18 nM, respectively]. Receptor-mediated [ Ca2+]i increase
was dose-dependenwt ith a 50% effective concentration (EC,,)
of N lo-lo M. The increment in [Ca”‘]i was due to internal
release and influx across the plasma membrane. Prior treatment
of ANP or CNP (10q7 M) did not markedly affect a post application
of either ANP or CNP. The truncated analogue of ANP,
C-ANP-(4-23), which preferentially binds to clearance receptors,
elicited an increase in [Ca”+]i (82 & 1 to 427 t 41 nM).
8-Bromoguanosine 3’,5’-cyclic monophosphate (8-BrcGMP)
did not alter [Ca”+]i, but pretreatment of CTAL cells with
8-BrcGMP for 30 min before agonist treatment prevented
ANP-induced Ca2+ signals [83 t 5 (basal) to 88 t 5 nM (stimulated)].
These results are evidence for the existence of clearance
ANP receptors in CTAL cells that may have biological functions
and clearance. The functional responseso f these signal
interactions may have important consequenceosn hormone actions
with the CTAL.
porcine thick ascending
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