scholarly journals Hypertension Secondary to PHPT: Cause or Coincidence?

2011 ◽  
Vol 2011 ◽  
pp. 1-6 ◽  
Author(s):  
Helmut Schiffl ◽  
Susanne M. Lang
Keyword(s):  
Cardiovascular Reactivity ◽  
Vascular Reactivity ◽  
Cytosolic Calcium ◽  
Free Calcium ◽  
Normal Blood Pressure ◽  
Cytosolic Free Calcium ◽  
Hypertensive Patients ◽  
Before And After ◽  
Underlying Mechanisms ◽  
Normal Controls

Primary hyperparathyroidism (PHPT) may be associated with arterial hypertension. The underlying mechanisms are not fully understood and reversibility by parathyroid surgery is controversial. This study aimed to characterize pressor hormones, vascular reactivity to norepinephrine, and cytosolic-free calcium in platelets in 15 hypertensive patients with hypercalcaemic PHPT before and after successful parathyroidectomy and to compare them with 5 pre-hypertensive patients with normocalcaemic PHPT, 8 normotensive patients with hypercalcaemic PHPT and 15 normal controls. Hypertensive patients with hypercalcaemic PHPT had slightly higher levels of pressor hormones (), enhanced cardiovascular reactivity to norepinephrine () and increased cytosolic calcium in platelets () than controls. Pre-hypertensive patients with normocalcaemic PHPT had intermediate values of increased cardiovascular reactivity and cytosolic calcium. Normotensive patients with hypercalcaemic PHPT and normotensive controls had comparable pressor hormone concentrations and intracellular calcium levels. Successful parathyroidectomy was associated with normal blood pressure values and normalisation of pressor hormone concentrations, cardiovascular pressor reactivity and cytosolic free calcium. Our results suggest that parathyroid hypertension is mediated/maintained, at least in part, by functional alterations of vascular smooth muscle cells and can be cured by parathyroidectomy in those patients who do not have primary hypertension.

Platelet Cytosolic Free Calcium in Essential Hypertension: Responses to Vasopressin

1989 ◽  
Vol 77 (2) ◽  
pp. 183-188 ◽  
Author(s):  
A. F. Dominiczak ◽  
J. J. Morton ◽  
G. Murray ◽  
P. F. Semple
Keyword(s):  
Essential Hypertension ◽  
Arginine Vasopressin ◽  
Calcium Concentration ◽  
Systolic Pressure ◽  
Extracellular Calcium ◽  
Free Calcium ◽  
Cytosolic Free Calcium ◽  
Hypertensive Patients ◽  
Free Calcium Concentration ◽  
The Difference

1. Resting and stimulated free calcium concentrations have been measured in platelets loaded with the fluorescent probe quin2 from 30 patients with essential hypertension and from 30 age-matched controls. 2. Cytosolic free calcium concentrations were 94.6 ± 2.7 (mean ± sem) in the hypertensive group and 91.7 ± 2.8 nmol/l in the normotensive group, the difference was not significant. 3. Arginine vasopressin caused a transient increase in platelet free calcium concentration in all subjects. In the presence of extracellular calcium the increase was significantly higher in the control subjects than in the hypertensive patients (P = 0.005). In the absence of extracellular calcium, arginine vasopressin caused much smaller increases, and there was then no difference between the responses of the two groups. 4. Platelet free calcium concentrations were measured again in 13 patients after 8 weeks treatment with either verapamil (n = 6) or atenolol (n = 7). The reductions in systolic pressure after drug treatment were correlated with the changes in cytosolic free calcium concentrations (r = 0.75, P < 0.01).

Angiotensin II causes sustained elevations in cytosolic calcium in glomerulosa cells

1988 ◽  
Vol 255 (3) ◽  
pp. E338-E346 ◽  
Author(s):  
R. E. Kramer
Keyword(s):  
Angiotensin Ii ◽  
Calcium Concentration ◽  
Cytosolic Calcium ◽  
Calcium Signal ◽  
Free Calcium ◽  
Cytosolic Free Calcium ◽  
Cytosolic Calcium Concentration ◽  
Free Calcium Concentration ◽  
Cytosolic Free Calcium Concentration ◽  
Glomerulosa Cells

Studies were conducted to examine the effects of angiotensin II on cytosolic free calcium concentration in bovine adrenal glomerulosa cells maintained in primary culture. The calcium indicator, fura-2, and discontinuous dual-wavelength fluorescence spectroscopy were used to measure cytosolic free calcium in superfused adherent cell monolayers. Basal cytosolic free calcium concentration was 63.7 +/- 3.3 nM. The threshold concentration for angiotensin II-stimulated increases in cytosolic calcium was 10(-14)-10(-13) M, and maximal elevation of cytosolic calcium was produced by 10(-9) M angiotensin II. Angiotensin II (10(-13) M) produced a gradual increase in cytosolic calcium concentration that plateaued after 3-5 min of superfusion at a level approximately 1.2 times that of control cells. The calcium signal invoked by a maximal concentration (10(-9) M) of angiotensin II, in contrast, was characterized by an immediate, intense (approximately 8-fold) increase in cytosolic calcium concentration that decayed within 5 min to a lower, but sustained, level 2.5-3 times that of control cells. The calcium signals invoked by intermediate concentrations (10(-12)-10(-10) M) of angiotensin II exhibited dose-dependent increases in magnitude and a gradual transition in nature between those invoked by threshold and maximal concentrations of the peptide. The effect of angiotensin II to increase cytosolic calcium concentration was accompanied by an increase in aldosterone output. The increase in steroidogenesis was most closely correlated with the magnitude of the initial calcium signal. At high concentrations (10(-10) and 10(-9) M) of angiotensin II, there was a clear dissociation between aldosterone output and the magnitude of the sustained calcium signal.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Calcium Regulates the Association between Mitochondria and a Smooth Subdomain of the Endoplasmic Reticulum

2000 ◽  
Vol 150 (6) ◽  
pp. 1489-1498 ◽  
Author(s):  
Hui-Jun Wang ◽  
Ginette Guay ◽  
Liviu Pogan ◽  
Remy Sauvé ◽  
Ivan R. Nabi
Keyword(s):  
Confocal Microscopy ◽  
Mdck Cells ◽  
Close Association ◽  
Cytosolic Calcium ◽  
Free Calcium ◽  
Autocrine Motility Factor ◽  
Cytosolic Free Calcium ◽  
Motility Factor ◽  
Rat Liver Cytosol ◽  
Close Contacts

Association between the ER and mitochondria has long been observed, and the formation of close contacts between ER and mitochondria is necessary for the ER-mediated sequestration of cytosolic calcium by mitochondria. Autocrine motility factor receptor (AMF-R) is a marker for a smooth subdomain of the ER, shown here by confocal microscopy to be distinct from, yet closely associated with the calnexin- or calreticulin-labeled ER. By EM, smooth ER AMF-R tubules exhibit direct interactions with mitochondria, identifying them as a mitochondria-associated smooth ER subdomain. In digitonin-permeabilized MDCK cells, the addition of rat liver cytosol stimulates the dissociation of smooth ER and mitochondria under conditions of low calcium. Using BAPTA chelators of various affinities and CaEGTA buffers of defined free Ca2+ concentrations and quantitative confocal microscopy, we show that free calcium concentrations &lt;100 nM favor dissociation, whereas those &gt;1 μM favor close association between these two organelles. Therefore, we describe a cellular mechanism that facilitates the close association of this smooth ER subdomain and mitochondria when cytosolic free calcium rises above physiological levels.

scholarly journals Efek Kombinasi Ramuan Jamu Terhadap Tekanan Darah dan Kolesterol Pasien di Rumah Riset Jamu Hortus Medicus

2018 ◽  
Vol 1 (3) ◽  
pp. 152-157
Author(s):  
Peristiwan Ridha Widhi Astana ◽  
Fajar Novianto ◽  
Agus Triyono
Keyword(s):  
Blood Pressure ◽  
Combination Therapy ◽  
Systolic Blood Pressure ◽  
Health Problem ◽  
Retrospective Cohort ◽  
Normal Blood Pressure ◽  
Hypertensive Patients ◽  
Cholesterol Levels ◽  
Before And After ◽  
Paired T Test

Hipertensi dan hiperkolesterolemia masih merupakan masalah di bidang kesehatan. Penanganan pasien hipertensi yang disertai hiperkolesterolemia memerlukan perhatian khusus. Di Rumah Riset Jamu (RRJ) terdapat banyak pasien hipertensi dengan hiperkolesterolemia yang diterapi menggunakan kombinasi ramuan jamu antihipertensi dan antihiperkolesterolemia. Penelitian ini bertujuan untuk mengetahui efek kombinasi ramuan jamu tersebut dalam menurunkan tekanan darah dan kadar kolesterol. Penelitian ini dilakukan menggunakan metode kohort retrospektif. Sampel didapatkan dari data rekam medik pasien hipertensi yang disertai hiperkolesterolemia di RRJ Hortus Medicus tahun 2017. Subjek penelitian ini adalah pasien yang berusia 20-65 tahun dan telah menjalani terapi kombinasi ramuan jamu antihipertensi dan antihiperkolesterol minimal 28 hari. Analisis dilakukan dengan membandingkan tekanan darah dan kadar kolesterol pasien pada hari ke-0 dan hari ke-28 masing-masing menggunakan uji t berpasangan. Sebanyak 223 data pasien didapatkan. Setelah 28 hari, terdapat 74 orang yang berhasil mencapai tekanan darah normal dan 115 orang berhasil mencapai kadar kolesterol normal. Tekanan darah sistolik berbeda secara signifikan antara sebelum dan setelah pemberian ramuan jamu, p=0,000. Demikian juga tekanan darah diastolik berbeda secara signifikan antara sebelum dan setelah pemberian ramuan jamu p=0,005. Kadar kolesterol di dalam darah pasien juga berbeda secara signifikan antara sebelum dan setelah pemberian ramuan jamu, p=0,014. Berdasarkan hasil di atas, dapat disimpulkan bahwa pemberian kombinasi ramuan jamu antihipertensi dan antihiperkolesterolemia selama 28 hari dapat menurunkan tekanan darah dan kadar kolesterol pasien secara signifikan.   Hypertension and hypercholesterolemia are still a health problem. Treatment of hypertensive patients comorbid with hypercholesterolemia requires special attention. At the Jamu Research House (RRJ) there are many hypertensive patients with hypercholesterolemia who are treated using a combination of antihypertensive and antihypercholesterolemic herbs. This study aimed to determine the effect of the combination of jamu in lowering blood pressure and cholesterol levels. This study was conducted using a retrospective cohort method. Samples were obtained from medical record of hypertensive patients comorbid with hypercholesterolemia at RRJ Hortus Medicines in 2017. The subjects of this study were patients aged 20-65 years and had undergone a combination therapy of antihypertensive and antihypercholesterolemicjamu at least 28 days. The analysis was carried out by comparing the blood pressure and cholesterol levels of patients on day 0 and day 28 using paired t test. A number of 223 patient data were obtained. After 28 days, there were 74 people who reach normal blood pressure and 115 people achieve normal cholesterol levels. Systolic blood pressure was significantly different between before and after the administration of jamu, p = 0,000. Likewise, diastolic blood pressure was significantly different between before and after the administration of jamu with p = 0.005. Cholesterol levels in the patient's blood also differed significantly between before and after administration of jamu formula, p = 0.014. Based on the above results, it can be concluded that the combination of antihypertensive and antihypercholesterolemic jamu for 28 days significantly reduced blood pressure and patient cholesterol levels

Effect of 17 β-estradiol on calcium response to phytohaemagglutinin in human lymphocytes

1990 ◽  
Vol 10 (1) ◽  
pp. 73-78 ◽  
Author(s):  
Tiziana Bellini ◽  
Diana Degani ◽  
Maurizio Matteuzzi ◽  
Franco Dallocchio
Keyword(s):  
Cell Surface ◽  
Steroid Hormones ◽  
Human Lymphocytes ◽  
Cytosolic Calcium ◽  
Free Calcium ◽  
Cytosolic Free Calcium ◽  
Calcium Response ◽  
Pre Treatment ◽  
Preincubation Time ◽  
Estradiol Concentration

Pre-treatment of human lymphocytes with 17 β-estradiol diminishes the increase in concentration of cytosolic free calcium after stimulation with phytohaemagglutinin. The effect is dependent on 17 β-estradiol concentration and on the preincubation time. The effect is not due to an interaction between 17 β-estradiol and phytohaemagglutinin, but appears to be a consequence of the binding of the hormone to the cell surface. The effect is specific for 17 β-estradiol, since the α isomer and other steroid hormones (progesterone, testosterone, diethylstilbestrol and 5α-androstan), have no effect. Since the effect of the 17 β-estradiol can be suppressed by treatment of lymphocytes with ouabain, it appears that the effect of estradiol on the rise of cytosolic calcium induced by phytohaemagglutinin is mediated by the (Na, K)-ATPase.

Cytosolic free calcium regulation in response to acute changes in intracellular pH in vascular smooth muscle

1993 ◽  
Vol 264 (4) ◽  
pp. C932-C943 ◽  
Author(s):  
D. C. Batlle ◽  
R. Peces ◽  
M. S. LaPointe ◽  
M. Ye ◽  
J. T. Daugirdas
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Intracellular Ph ◽  
Cytosolic Calcium ◽  
Free Calcium ◽  
Cytosolic Free Calcium ◽  
Intracellular Store ◽  
Acute Changes ◽  
Free Media ◽  
Intracellular Alkalinization

This study examined the mechanisms whereby alterations of intracellular pH (pHi) impact on free cytosolic calcium (Cai2+) in cultured rat aortic vascular smooth muscle cells (VSMC) assayed in the presence of HCO3/CO2. Rapid cell alkalinization, effected by the exposure to NH4Cl or removal of CO2 from the superfusate, produced a rapid increase in Cai2+. The rise in Cai2+ was markedly diminished when sarcoplasmic reticulum (SR) Ca2+ stores had been depleted by prior exposure to arginine vasopressin (AVP) in Ca(2+)-free media or when SR release and reuptake of Ca2+ were blocked by the addition of 3,4,5-trimethoxybenzoic acid 8-(diethylamino)octyl ester (TMB-8), but was unaffected by the removal of external Ca2+ or inhibition of Ca2+ entry using NiCl2. Cell acidification also resulted in a rapid increase in Cai2+. This Cai2+ increase was most apparent when pHi was very low (< 6.6) and was unaffected by removal of external Ca2+ or NiCl2 addition. Unlike the effect of cell alkalinization, the increase in Cai2+ associated with cell acidification was not prevented by pretreatment with AVP or TMB-8. We conclude that, in cultured VSMC, acute intracellular alkalinization and, to a lesser extent, acidification result in release of Ca2+ from internal stores. Alkalinization increases Cai2+ by promoting its release from a store which is AVP and TMB-8 sensitive, most likely the SR. Cell acidification increases Cai2+ from an intracellular store(s) that is neither AVP nor TMB-8 sensitive. The increase in Cai2+ produced by cell acidification may be explained on the basis of cell buffering such that, as cytosolic H+ increases, it displaces Cai2+ from internal buffers with similar affinities for Ca2+ and H+.

scholarly journals Influence of the calcium-sensitive fluorophore, Quin 2, on platelet function

Blood ◽  
1986 ◽  
Vol 67 (2) ◽  
pp. 354-361 ◽  
Author(s):  
GH Rao ◽  
JD Peller ◽  
CP Semba ◽  
JG White
Keyword(s):  
Platelet Function ◽  
Light Emission ◽  
Cytosolic Calcium ◽  
Functional Restoration ◽  
Calcium Flux ◽  
Free Calcium ◽  
Cytosolic Free Calcium ◽  
Experimental Conditions ◽  
Calcium Dependent ◽  
Dose Dependent Increase

Abstract Recent investigations using Quin 2, a fluorophore used to monitor cytosolic free calcium shifts, have shown that strong agonists cause a dramatic dose-dependent increase in platelet fluorescence. However, weak agonists stimulated little or no increase in light emission of Quin 2-loaded platelets, suggesting that calcium flux is not involved in activation by these agents. The present study has sought an alternative explanation for the failure of weak stimuli to cause a rise in cytosolic free calcium in platelets containing Quin 2. Conditions used to prepare, wash, load, gel-filter, and evaluate the fluorophore- filled cells were examined for their compatibility with retention of sensitivity to activation by weak agonists. The technique used to measure shifts in cytosolic calcium with Quin 2 requires multiply washed, unstirred platelets. Under these conditions, platelets do not aggregate or secrete in response to weak agonists. Quin 2, at concentrations greater than 40 mumol/L, inhibits the response of platelets to strong agonists, and completely blocks their reaction to weak agonists. Quin 2 inhibition of platelet function appears related to high buffering capacity for free calcium, although other mechanisms cannot be ruled out. This suggestion is supported by the observation that Quin 2-induced blockade can be overcome by membrane modulation, which is a calcium-dependent process. However, since both agonists are weak, significant elevation in cytosolic calcium concurrent with functional restoration could not be demonstrated under the experimental conditions used for monitoring calcium. Thus, the conditions used to prepare platelets for Quin 2 evaluation and Quin 2 itself appear to be responsible for the failure of weak agonists to cause evidence of a calcium shift in fluorophore-loaded cells.

The relation of elevation of cytosolic free calcium to activation of membrane conductance in rat parotid acinar cells

1989 ◽  
Vol 237 (1286) ◽  
pp. 99-107 ◽  
Keyword(s):  
Outward Current ◽  
Membrane Conductance ◽  
Acinar Cells ◽  
Cytosolic Calcium ◽  
Free Calcium ◽  
Muscarinic Agonists ◽  
Cytosolic Free Calcium ◽  
Voltage Dependent ◽  
Inward Currents ◽  
Rat Parotid

The relation between elevation of cytosolic free calcium and activation of membrane conductance has been studied in single acinar cells of the rat parotid. Outward and inward currents are activated by calcium elevation and oscillate in phase with oscillations of cytosolic calcium. The outward current results from activation of a large unit-conductance Ca 2+ and voltage-dependent K + channel, whereas the inward current is most likely carried predominantly by Cl - . Both these conductances have been previously described in exocrine cells. Buffering calcium at resting levels eliminated current responses to muscarinic agonists, suggesting that calcium is the only significant second messenger involved in the short-term control of this conductance by acetylcholine.

Resting and stimulated cytosolic free calcium levels in neutrophils from patients with Bartter's syndrome

1987 ◽  
Vol 72 (4) ◽  
pp. 483-488 ◽  
Author(s):  
Francesco Di Virgilio ◽  
Lorenzo Calò ◽  
Salvatore Cantaro ◽  
Silvana Favaro ◽  
Antonio Piccoli ◽  
...  
Keyword(s):  
Free Calcium ◽  
Healthy Controls ◽  
Bartter’S Syndrome ◽  
Bartter's Syndrome ◽  
Chemotactic Peptide ◽  
Cytosolic Free Calcium ◽  
Fluorescent Indicator ◽  
Activated Neutrophils ◽  
Normal Controls

1. Cytosolic free calcium concentrations ([a2+]i) were measured in resting and chemotactic peptide-activated neutrophils from eight patients with Bartter's syndrome and compared with levels determined in neutrophils isolated from healthy controls. 2. [Ca2+]i was measured with the intracellular trappable fluorescent indicator Quin2. The synthetic tripeptide formylmethionyl-leucyl-phenylalanine (fMet-Leu-Phe) was used as a stimulant. 3. No difference was found in resting [Ca2+]i between neutrophils from normal controls and those from patients with Bartter's syndrome. 4. On the contrary increases in [Ca2+]i stimulated by fMet-Leu-Phe concentrations higher than 10−8 mol/l were significantly less in neutrophils from patients with Bartter's syndrome. 5. It is suggested that neutrophils from patients affected by Bartter's syndrome exhibit an intrinsic anomaly in the mechanism responsible for intracellular Ca2+ mobilization.

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