Calcium channels contribute to the decrease in blood pressure of pregnant rats

2002 ◽  
Vol 282 (2) ◽  
pp. H665-H671 ◽  
Author(s):  
May Simaan ◽  
Chanterelle Cadorette ◽  
Matthieu Poterek ◽  
Jean St-Louis ◽  
Michèle Brochu
Keyword(s):  
Blood Pressure ◽  
Calcium Channels ◽  
Calcium Channel ◽  
Plasma Renin ◽  
Late Pregnancy ◽  
Pregnant Rats ◽  
Affect Body Weight ◽  
Voltage Dependent ◽  
Voltage Dependent Calcium Channels ◽  
Calcium Channel Activator

Pregnancy is associated with hemodynamic changes such as reduced vascular resistance and blood pressure. We reported that, during late pregnancy, the activity of voltage-dependent calcium channels (VDCC) is altered in the adrenal cortex and vascular smooth muscle. These observations suggested that the late pregnancy-induced decrease in blood pressure is linked to diminished VDCC function. We attempted to prevent pregnancy-induced reduced blood pressure with a calcium channel activator (CGP 28392) in pregnant rats and to mimic it by administration of a calcium channel blocker (nifedipine) to nonpregnant rats. Treatment was given from the 15th day of gestation for 7 days. The systolic blood pressure of CGP 28392-treated pregnant rats rose transiently for 2 days and then declined toward values of nontreated pregnant controls, although remaining higher. However, nonpregnant rats maintained their high arterial pressure throughout CGP 28392 treatment. Nifedipine lowered the blood pressure in nonpregnant rats to values of nontreated term-pregnant controls. Both agents did not affect body weight, water or food intake, plasma renin activity, and plasma aldosterone or corticosterone levels. Nifedipine and CGP 28392 treatment of nonpregnant and pregnant animals, respectively, did not modify the response of aortic rings to KCl. These results show that VDCC activation caused hypertension, which modified the extent of the decrease in blood pressure at the end of pregnancy.

scholarly journals Comparison of the effects of L-type calcium channel antagonist Amlodipine with L/N-type calcium channel antagonist Cilnidipine on blood pressure, heart rate, proteinuria and lipid profile in hypertensive patients

2016 ◽  
Vol 15 (3) ◽  
pp. 460-465
Author(s):  
Kiran Kumar Singal ◽  
Neerja Singal ◽  
Abhinav Gupta ◽  
Akash Garg ◽  
Ravi Kumar
Keyword(s):  
Blood Pressure ◽  
Calcium Channel ◽  
Calcium Channel Antagonist ◽  
Total Cholesterol Level ◽  
Medical Science ◽  
Reflex Tachycardia ◽  
Before And After ◽  
Voltage Dependent ◽  
Amlodipine Group ◽  
Voltage Dependent Calcium Channels

Background: Cilnidipine is a novel and unique 1,4-dydropyridine derivative calcium antagonist that exerts potent inhibitory actions not only on L-type but also on N-type voltage dependent calcium channels. Blockade of the neural N-type calcium channel inhibits the secretion of norepinephrine from peripheral neural terminals and depresses sympathetic nervous system activity.Objective and methods: The purpose of this study was to assess the effect of Cilnidipine and Amlodipine on blood pressure (BP) levels. We did BP monitoring before and after once-daily use of Cilnidipine and Amlodipine in 100 hypertensive patients.Results: Both drugs significantly reduced systolic BP (SBP) and diastolic BP (DBP). However, the reductions in pulse rate (PR) were significantly greater in the Cilnidipine group than the Amlodipine group. N-type calcium channel blockade by Cilnidipine may not cause reflex tachycardia, and may be useful for hypertensive treatment.Conclusion: There was significant reduction in proteinuria with Clindipine as compared to Amlodipine. However, there were no significant change in total cholesterol level in diabetes and non-diabetics in both the group.Bangladesh Journal of Medical Science Vol.15(3) 2016 p.460-465

Dihydropyridine-sensitive single calcium channels in airway smooth muscle cells

1990 ◽  
Vol 259 (6) ◽  
pp. L468-L480 ◽  
Author(s):  
J. F. Worley ◽  
M. I. Kotlikoff
Keyword(s):  
Smooth Muscle ◽  
Calcium Channels ◽  
Smooth Muscle Cells ◽  
Calcium Channel ◽  
Airway Smooth Muscle ◽  
Muscle Cells ◽  
Membrane Depolarization ◽  
Airway Smooth Muscle Cells ◽  
Voltage Dependent ◽  
Voltage Dependent Calcium Channels

We have identified and characterized single voltage-dependent calcium channels in both acutely dissociated rat bronchial and cultured human tracheobronchial smooth muscle cells using the patch-clamp technique. In both cell types, on-cell membrane patches displayed unitary currents selective for barium ions and exhibited one conductance level (21–26 pS), and the open state probability was increased by membrane depolarization. Unitary barium currents were enhanced by the calcium channel selective agonist, BAY R 5417, and inhibited by the dihydropyridine calcium channel antagonist, nisoldipine (apparent inhibition constant less than 100 nM). Moreover, the degree of nisoldipine inhibition of the rat bronchial smooth muscle channels was increased with membrane depolarization in a manner consistent with the drug interacting with highest affinity to the inactivated channel state. In addition, the sensitivity to BAY R 5417 augmentation and nisoldipine inhibition of depolarization-induced tonic force of intact rat bronchial ring segments was in close agreement to the single channel results. Thus these data suggest that activation of voltage-dependent calcium channels can influence airway contraction and that dihydropyridines may be effective modulators of depolarization-induced increases in bronchial tone. We conclude that both rat and human airway smooth muscle cells have high-conductance voltage-dependent calcium channels that interact in a predictable manner with dihydropyridines and are similar to voltage-dependent calcium channels observed in other smooth muscle cells.

Dissection of the Calcium Channel Domains Responsible for Modulation of Neuronal Voltage-Dependent Calcium Channels by G Proteins

1999 ◽  
Vol 868 (1 MOLECULAR AND) ◽  
pp. 160-174 ◽  
Author(s):  
ANNETTE C. DOLPHIN ◽  
KAREN M. PAGE ◽  
NICHOLAS S. BERROW ◽  
GARY J. STEPHENS ◽  
CARLES CANTI
Keyword(s):  
Calcium Channels ◽  
Calcium Channel ◽  
G Proteins ◽  
Voltage Dependent ◽  
Voltage Dependent Calcium Channels

Functional alteration of dihydropyridine-sensitive Ca2+ channels in the adrenal glomerulosa of pregnant rats

2000 ◽  
Vol 278 (5) ◽  
pp. E925-E932 ◽  
Author(s):  
May Simaan ◽  
Serge Picard ◽  
Jean St-Louis ◽  
Michèle Brochu
Keyword(s):  
Calcium Channels ◽  
Zona Glomerulosa ◽  
Pregnant Rats ◽  
Western Blots ◽  
Pregnant Rat ◽  
Voltage Dependent ◽  
Functionally Impaired ◽  
Voltage Dependent Calcium Channels ◽  
Conformational Alteration ◽  
Functional Alteration

Our previous work on aldosterone secretion suggested that dihydropyridine-sensitive calcium channels, one type of voltage-dependent calcium channels (VDCC), are functionally impaired in adrenal capsule preparations from the pregnant rat. The aim of this study was to determine whether, during pregnancy, the density and/or activity of these channels is altered in the adrenal zona glomerulosa. These VDCC measured with [3H]nitrendipine binding were not different between membrane preparations of nonpregnant and pregnant rats. Western blots were performed using two different antibodies, a polyclonal (PcAb) directed against the α1-subunit of VDCC and a monoclonal (McAb) that recognizes an intracellular domain of that protein. McAb immunoreactivity showed a significant decrease in preparations from pregnant rats, whereas no difference was observed with PcAb. VDCC activity was estimated by45Ca2+ uptake in isolated adrenal cortex and by intracellular calcium concentration ([Ca2+]i) in adrenal glomerulosa cells with the Ca2+ probe fura PE3. These measurements revealed that KCl stimulation produced greater Ca2+ influx in nonpregnant than in pregnant rats. Nifedipine (a blocker of VDCC) inhibited this stimulation only in nonpregnant rats, whereas BAY K 8644 (an activator of VDCC) increased Ca2+ influx in pregnant rats only. These data suggest that, during pregnancy, the altered regulation of calcium homeostasis in adrenal glomerulosa is linked to a conformational alteration of VDCC.

scholarly journals Partners in Crime: Towards New Ways of Targeting Calcium Channels

2019 ◽  
Vol 20 (24) ◽  
pp. 6344 ◽  
Author(s):  
Lucile Noyer ◽  
Loic Lemonnier ◽  
Pascal Mariot ◽  
Dimitra Gkika
Keyword(s):  
Calcium Channels ◽  
Calcium Channel ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Interaction Domain ◽  
Domain Structures ◽  
Voltage Dependent ◽  
Voltage Dependent Calcium Channels ◽  
Transient Receptor ◽  
Partner Proteins

The characterization of calcium channel interactome in the last decades opened a new way of perceiving ion channel function and regulation. Partner proteins of ion channels can now be considered as major components of the calcium homeostatic mechanisms, while the reinforcement or disruption of their interaction with the channel units now represents an attractive target in research and therapeutics. In this review we will focus on the targeting of calcium channel partner proteins in order to act on the channel activity, and on its consequences for cell and organism physiology. Given the recent advances in the partner proteins’ identification, characterization, as well as in the resolution of their interaction domain structures, we will develop the latest findings on the interacting proteins of the following channels: voltage-dependent calcium channels, transient receptor potential and ORAI channels, and inositol 1,4,5-trisphosphate receptor.

Molecular characterization of renal calcium channel beta-subunit transcripts

1995 ◽  
Vol 268 (3) ◽  
pp. F525-F531 ◽  
Author(s):  
A. S. Yu ◽  
M. Boim ◽  
S. C. Hebert ◽  
A. Castellano ◽  
E. Perez-Reyes ◽  
...  
Keyword(s):  
Calcium Channels ◽  
Calcium Channel ◽  
Rat Kidney ◽  
Beta Subunit ◽  
Kidney Cortex ◽  
Calcium Excretion ◽  
Gene Transcript ◽  
Degenerate Primers ◽  
Voltage Dependent ◽  
Voltage Dependent Calcium Channels

An apical, hormone-regulated, calcium entry channel in the distal convoluted tubule and/or connecting tubule (DCT/CNT) is thought to play an important role in controlling renal calcium excretion. We previously identified a gene transcript encoding the pore-forming alpha 1-subunit of a calcium channel (alpha 1A, or CaCh4) which may be a candidate for such a molecule. The properties of voltage-dependent calcium channels are known to be modulated by their beta-subunits. To identify the accessory beta-subunit of DCT/CNT calcium channels, degenerate primers based on published beta-subunit sequences were used to amplify rat kidney cDNA by the polymerase chain reaction (PCR), and the products were subcloned and sequenced. Alternatively spliced transcripts of three beta-subunit genes (beta 2, beta 3, and beta 4) were identified. Northern blot analysis indicated that beta 4-subunit is preferentially expressed in kidney cortex. Transcripts of all three beta-subunit genes were detected by PCR in microdissected nephron segments, but only beta 4-subunit was found in DCT/CNT. As the beta 4- and alpha 1A-subunits colocalize to the DCT/CNT, we hypothesize that they may be constituent subunits of a renal calcium channel regulated by a hormone(s).

scholarly journals Properties and modulation of cardiac calcium channels

1986 ◽  
Vol 124 (1) ◽  
pp. 191-201 ◽  
Author(s):  
H. Reuter ◽  
S. Kokubun ◽  
B. Prod'hom
Keyword(s):  
Cyclic Amp ◽  
Calcium Channels ◽  
Calcium Channel ◽  
Cardiac Cells ◽  
Cellular Functions ◽  
Beta Adrenoceptor ◽  
Excitable Membranes ◽  
Rat Hearts ◽  
Voltage Dependent ◽  
Voltage Dependent Calcium Channels

Voltage-dependent calcium channels are widely distributed in excitable membranes and are involved in the regulation of many cellular functions. These channels can be modulated by neurotransmitters and drugs. There is one particular type of calcium channel in cardiac cells (L-type) whose gating is affected in different ways by beta-adrenoceptor and 1,4-dihydropyridine agonists. We have analysed single calcium channel currents (i) in myocytes from rat hearts in the absence and presence of isoproterenol or 8-bromo-cAMP. We have found that both compounds have similar effects on calcium channel properties. They increase the overall open state probability (po) of individual calcium channels while i remains unaffected. Analysis of the gating kinetics of calcium channels showed: a slight increase in the mean open times of calcium channels, a reduction in time intervals between bursts of channel openings, an increase in burst length and a prominent reduction in failures of calcium channels to open upon depolarization. These kinetic changes caused by isoproterenol and 8-bromo-cAMP can account for the increase in po. Since the macroscopic calcium current, ICa, can be described by ICa = N X po X i, the increase in po accounts for the well-known increase in ICa by beta-adrenergic catecholamines. Cyclic AMP-dependent phosphorylation of calcium channels is a likely metabolic step involved in this modulation. Another class of drug that modulates calcium channel gating is the 1,4-dihydropyridines which can either enhance or reduce ICa, either by prolonging the open state of the channels or by facilitating the inactivated state. Both effects depend strongly on membrane potential and are independent of cyclic AMP-dependent phosphorylation reactions.

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