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PubMed1971

Adrenal catecholamine secretion during stimulation of the nasal mucous membrane in the rabbit.

1. Left adrenal venous blood was collected in anaesthetized rabbits and analysed for catecholamine content by either a fluorimetric technique or a bio-assay method using the blood pressure of the pithed rat.2. Stimulation of the nasal mucous membrane with ether vapour or water caused apnoea, bradycardia, a rise in arterial blood pressure and an increase in adrenal medullary catecholamine secretion.3. During the pre-stimulation control periods adrenaline constituted 66% of the total catecholamine present in adrenal venous blood and noradrenaline 34%. These proportions altered during stimulation of the nasal mucous membrane to 72 and 28% respectively. Electrical stimulation of the left splanchnic nerve produced a secretion composed almost entirely of adrenaline.4. The increased catecholamine output elicited during stimulation of the nose occurred in animals whose pulmonary ventilation was maintained constant by means of a pump. It was abolished, however, by local anaesthesia of the nasal passages or by surgical division of the left splanchnic nerve.5. The increased secretion of catecholamines is therefore reflex in nature, and evidence is presented that it is the result of a primary reflex from the nose.

Adrenal Medulla↗
PubMed1986

Facilitation of transmitter action on catecholamine output by cardiac glycoside in perfused adrenal gland of guinea-pig.

Effects of K+ deprivation and ouabain on catecholamine secretion evoked by splanchnic nerve stimulation (5 Hz), ACh (10(-5) M) and/or excess K+ (56 mM) were studied in isolated and perfused adrenal glands of guinea-pig. Exposure to K+-free Locke solution initially reduced and later enhanced catecholamine secretion sequentially evoked by splanchnic nerve stimulation and ACh. The enhancement attained a maximum, 185% in magnitude of the corresponding control response at 35 min for splanchnic nerve stimulation and 135% at 65 min for ACh after the start of exposure to K+-free solution. Ouabain (10(-5) M) caused a larger increase in the evoked catecholamine section than K+ deprivation did. The maximum effect was obtained from 40 to 50 min after the start of exposure to ouabain in which the magnitude of responses to splanchnic nerve stimulation, excess K+ and ACh was about 500, 400 and 300% of each control response, respectively. The effect of ouabain on the evoked catecholamine secretion increased as the concentration of extracellular Na+ was increased from 25 to 154 mM, regardless of the kind of stimuli. The ouabain-induced enhancement in the evoked responses was reversibly inhibited by removing Ca2+ from, or by adding Mg2+, Co2+ or Ni2+ to the perfusion medium. The ID50 values for Mg2+ were about 9.4 and 7.3 mM and those for Co2+ were 0.8 and 0.4 mM against ouabain on the responses to ACh and excess K+, respectively. The inhibitory effect of Mg2+ and Co2+ on the ouabain action was counteracted by increasing the concentration of Ca2+ from 2.2 to 8.8 mM in the perfusion medium. These results suggest that ouabain enhances catecholamine secretion evoked by splanchnic nerve stimulation, ACh and excess K+ by increasing the rate of Ca2+ influx through the ACh receptor linked Ca2+ channel and/or voltage-dependent Ca2+ channels on adrenal chromaffin cells of guinea-pig in a Na+-dependent manner.

Acetylcholine↗
PubMed1991

Release of glucose from the liver of fetal and postnatal sheep by portal vein infusion of catecholamines or glucagon.

1. The blood flow to the liver in fetuses near term, newborn and adult sheep was measured by the Fick principle, using radionuclide-labelled plastic microspheres, before and during infusion of adrenaline, noradrenaline or glucagon. 2. Glucose output and lactate consumption by the liver in sheep of each age group were calculated by application of the Fick principle using the concentration gradients of these metabolites measured in blood samples obtained, simultaneously with blood flow measurements, from catheters chronically implanted in the inflow and outflow vessels of the liver. 3. Catecholamines were infused into the portal vein of fetuses near term at a rate comparable with that at which they are known to be secreted in the sheep fetus during moderate to severe hypoxia. The cardiovascular and metabolic responses to these infusions were found to be comparable with those that occur in the fetus during hypoxia. 4. Catecholamines increased glucose output from the liver in all except the immediate post-partum animals. Catecholamines were less effective than glucagon in promoting glucose release. The mean increments in glucose output during adrenaline infusion were 0.055 +/- 0.015 mmol min-1 (100 g liver)-1 in the fetus, 0.122 +/- 0.024 mmol min-1 (100 g)-1 in the 2-week-old lambs, 0.078 +/- 0.019 mmol min-1 (100 g)-1 in young lambs and 0.049 +/- 0.012 mmol min-1 (100 g)-1 in the adult sheep. During glucagon infusion the mean glucose output increments were 0.146 +/- 0.023 mmol min-1 (100 g)-1 in the fetus, 0.274 +/- 0.085 mmol min-1 (100 g)-1 in the 2-week-old and young lambs and 0.180 +/- 0.054 mmol min-1 (100 g)-1 in the adult. Adrenaline was more potent than noradrenaline, suggesting that the major glycogenolytic response might be beta-receptor mediated. 5. In the immediate newborn period the output of glucose from the liver was high (0.20 +/- 0.05 mmol min-1 (100 g liver)-1 and was not statistically significantly increased by infusion either of glucagon or of catecholamines which resulted in similar increments of glucose output of about 0.128 +/- 0.133 mmol min-1 (100 g)-1. It is probable that the high output of glucose reflected the high endogenous circulating levels of catecholamines and glucagon in these animals at birth and that further infusions failed to add significantly to the already near-maximal glucose release.(ABSTRACT TRUNCATED AT 400 WORDS)

Age Factors↗
PubMed1977

Plasma catecholamine levels and cardiac rhythm before and after cardiac catheterisation.

Plasma catecholamine concentrations were estimated in a group of 17 fasting patients immediately before and 3 days after cardiac catheterisation. At both times electrocardiograms were recorded and blood pressures, heart rates, and respiration rates measured. Control catecholamine values were established in a group of 10 male and 10 female volunteers, bled at the same time of day under the same conditions of nutrition and posture. Levels of adrenaline and noradrenaline were increased substantially before catheterisation; 3 days later, the values were comparable to those of the control group, though still marginally higher. The increments in catecholamine levels were independent of sex and of the presence or otherwise of persistent supraventricular arrhythmias. In spite of the considerably raised catecholamine levels, electrocardiographic patterns remained unchanged, as did the other physiological values. The absence of any relation between enhanced catecholamine secretion and physiological effects is considered to be the result either of enhanced parasympathetic activity or of adaptation to a prolonged period of stress.

Adolescent↗
PubMed1984

Catecholamine-angiotensin II receptor interaction in primary cultures of rat brain.

Neuron-enriched primary cultures from 1-day-old rat brains have been used to study the influence of catecholamines on angiotension II receptors. Treatment of cultures with alpha-methyl-p-tyrosine caused a time- and concentration-dependent increase in the specific binding of 125I-angiotensin II and a decrease in neuronal norepinephrine and dopamine contents. A maximum increase of 75% in the binding and a decrease of 67% in catecholamine content was observed with 400 microM alpha-methyl-p-tyrosine. Removal of alpha-methyl-p-tyrosine from cultures resulted in the recovery of catecholamine levels and decrease in 125I-angiotensin II binding to control levels. In contrast, treatment of cultures with pargyline caused decreases in the binding of 125I-angiotensin II and increases in catecholamine levels in neuronal cultures. Scatchard analysis demonstrated that an increase in 125I-angiotensin II binding by alpha-methyl-p-tyrosine was due to an increase in the affinity of receptors for angiotensin II without changes in the number of angiotensin II binding sites. The results obtained here indicate that angiotensin II binding to neuron-enriched cultures is reciprocally related to the levels of neuronal catecholamines.

Angiotensin II↗
PubMed1995

PACAP stimulates catecholamine release from adrenal medulla: a novel noncholinergic secretagogue.

The secretory response of the adrenal medulla to pituitary adenylate cyclase-activating polypeptide (PACAP), a novel polypeptide with 68% structural homology to vasoactive intestinal polypeptide (VIP), was investigated in anesthetized rats by in vivo microdialysis. The injection of PACAP (1.5 nmol) caused a greater amount of increase in catecholamine concentration than carbachol (30 nmol) or VIP (30 nmol) in the dialysate for a period of 60 min. The ratios of norepinephrine to epinephrine in the dialysate after stimulation with these compounds showed no change from resting conditions. The simultaneous application of both nicotinic and muscarinic antagonists (10 mM mecamylamine and 1 mM atropine) eliminated the increase in catecholamine secretion induced by carbachol. In contrast, PACAP-induced catecholamine secretion was not inhibited by these cholinergic antagonists. These data led to the following conclusions: 1) PACAP was more potent than either carbachol or VIP in enhancing the secretion of catecholamine from the adrenal medulla, and 2) PACAP-induced catecholamine secretion was due to the direct action of PACAP on the adrenal medulla rather than an indirect action mediated by acetylcholine release. These results strongly suggest that PACAP is a noncholinergic secretagogue of the adrenal medulla in rats.

Adrenal Medulla↗
PubMed1982

Catecholamine effects on intracellular sodium activity and tension in dog heart.

Because catecholamines have been reported to stimulate the sodium pump and Na+-K+-ATPase in skeletal and cardiac muscle, we examined the effects of isoproterenol (0.2-1.0 X 10(-6) M) and norepinephrine (2-4 X 10(-7) M) on intracellular sodium activity (aiNa) and twitch tension in dog Purkinje strands and ventricular muscles, aiNa was measured with Na+-sensitive microelectrodes. During the initial rapid increase in tension induced by catecholamines in Purkinje strands, no changes in aiNa were found. After 5-10 min aiNa decreased by about 2 mM, coincident with a small decline in twitch tension. When the catecholamine was removed, tension declined rapidly to a level less than control. Recovery of tension to its control level less than control. Recovery of tension to its control level occurred simultaneously with recovery of aiNa. Comparable changes in aiNa occurred in ventricular muscle, but the biphasic effect of catecholamines on tension was not seen. These results are consistent with sodium pump stimulation in cardiac muscle. In Purkinje strands the resulting changes in aiNa may alter the direct positive inotropic effect of catecholamines, probably by influencing Na+-Ca2+ exchange.

Animals↗
PubMed1995

Catecholamine response to chronic ANG II infusion and its role in myocyte and coronary vascular damage.

Acute elevations in circulating angiotensin II (ANG II) are known to increase circulating norepinephrine (NE) levels. However, the time course of catecholamine release relative to chronic ANG II infusion is not known. Furthermore, it is unknown if this ANG II-induced catecholamine release is ANG II type 1 (AT1) receptor mediated or whether the increase in serum catecholamines is responsible for the myocyte and coronary vascular damage seen within the first 3 days of chronic ANG II infusion. Therefore, we examined the influence of chronic ANG II stimulation on serum catecholamine levels with and without AT1 blockade and the effect of beta-blockade on ANG II-induced myocyte and coronary vascular damage. The results indicate that NE release is AT1 mediated, but NE is not significantly elevated until day 4 of ANG II infusion after which it remains elevated. beta-Blockade prevented most ANG II-related myocyte necrosis and coronary vascular damage. Therefore, myocyte and coronary vascular damage do not appear to be related to increased serum NE levels, but instead may be due to the release of neural catecholamines within the heart.

Adrenergic beta-Antagonists↗
PubMed1982

Plasma catecholamines during hypoxemia in fetal lamb.

Changes in peripheral plasma catecholamines were studied during varying degrees of hypoxemia in fetal lambs of 95-140 days gestation. Epinephrine and norepinephrine concentrations were measured by radioenzymatic assay in plasma obtained simultaneously from the distal aorta and inferior vena cava in 15 chronically catheterized fetuses with the mother breathing 20, 10, or 8% oxygen mixtures. Levels of both epinephrine and norepinephrine increased significantly after 5 min of hypoxemia and showed a strong inverse exponential correlation with PO2 (P less than 0.001). Plasma norepinephrine always exceeded epinephrine concentrations (P less than 0.01). Resting arterial and venous catecholamine levels were not different, but during hypoxemia arterial levels of both epinephrine and norepinephrine exceeded venous levels significantly, suggesting the adrenal medulla as a major source of these substances. Hypoxemia led to fetal bradycardia, the degree of which moderated somewhat with extremely low oxygen tensions and associated very high catecholamine levels. Fetal blood pressure increased initially in proportion to norepinephrine levels but reached a plateau at concentrations higher than 10 ng/ml. Although concentrations of catecholamines were lower in the earlier gestation fetuses studied, similar qualitative relations between catecholamines and PO2 were evident at all gestational ages.

Animals↗
PubMed1987

Comparison of corticotropin-releasing factor and acetylcholine on catecholamine secretion in dogs.

To test whether corticotropin-releasing factor (CRF) is a secretagogue for adrenal secretion of catecholamines, a preparation was developed that permits measurement of adrenal venous output in response to in vivo arterial injection into the dog adrenal gland. Dogs were prepared with catheters in the lumboadrenal vein for monitoring adrenal blood flow and secretion rate of epinephrine and norepinephrine and in the lumboadrenal and inferior phrenic arteries for adrenal injection. Under pentobarbital anesthesia 48 h after surgery, dogs received a series of intra-adrenal injections that included acetylcholine (0.2-200 nmol), CRF (2.0-20.0 nmol), and diluent. There was a log dose-response relationship before epinephrine secretion and norepinephrine secretion to acetylcholine. Adrenal injection of CRF stimulated epinephrine and norepinephrine secretion at the highest dose tested (20 nmol). The response observed was equivalent to the response to 0.2 nmol acetylcholine. A similar dose of CRF given systemically produced hypotension without stimulating catecholamine responses. Adrenal catecholamine responses to acetylcholine were not augmented by addition of CRF. These findings show that arterial injection of CRF into the intact dog adrenal stimulates secretion of epinephrine and norepinephrine. However, the low potency of CRF relative to that of acetylcholine, the lack of a synergistic effect of CRF on catecholamine responses to acetylcholine, and the high dose of CRF required to achieve a response suggest that CRF does not function in the adrenal medulla as a physiologically important secretagogue for catecholamines.

Acetylcholine↗
PubMed1988

Correlation between catecholamine release and degree of acidotic stress in trout.

Exhaustive exercise in freshwater (FW) and seawater (SW) rainbow trout resulted in a marked and acute increase of plasma catecholamines. Immediately after exercise, epinephrine and norepinephrine concentrations in FW trout were 69 and 15 times the resting level, respectively; in SW trout, they were 46 and 11 times the resting value, respectively. Over the 1st h of recovery, the magnitude of the catecholamine surge in FW animals was about twice that of their SW counterparts. Correlated with this was an extracellular pH disturbance in FW trout, which was approximately twice as severe as in SW trout. Indeed, both the magnitudes and time courses of the plasma catecholamine responses were matched to those of the acid-base disturbances. Linear correlations were found to exist between the immediate depression of blood pH and the corresponding increases in plasma epinephrine and norepinephrine. We conclude that catecholamines are released into the plasma in proportion to the magnitude of the acid-base disturbance. The higher postexercise levels of plasma catecholamines in FW trout vs. SW appear to be a response to the greater acid-base disturbance in the FW animals.

Acclimatization↗
PubMed1988

Effects of chronic sinoaortic denervation on central vasopressin and catecholamine systems.

The objective of this study was to determine whether chronic arterial baroreceptor deficit induces time-related changes in central vasopressin (AVP) and catecholamine systems. Groups of sinoaortic-denervated (SAD) and sham-operated (SO) rats were studied 1, 3, 4, 7, and 14 days after surgery. Supraoptic (SON), paraventricular (PVN) and arcuate (ARC) nuclei, median eminence (ME) region, and A1 region of medulla were obtained by micropunch from frozen brain sections and assayed for AVP, tyrosine hydroxylase (TH) activity, catecholamines, and their metabolites, dihydroxyphenylethyleneglycol (DOPEG) and 2,5-dihydroxyphenylacetic acid (DOPAC). AVP concentration in SON and PVN was increased in 1-day-SAD rats, reduced in 3- and 4-day-SAD rats, equal and above control values in 7- and 14-day-SAD rats, respectively. TH activity was increased in SON and reduced in ME and ARC of 1- and 7-day-SAD rats. In SON, DOPEG was increased, whereas in ME all catecholamines and DOPEG and DOPAC were reduced in 1-day-SAD rats. ME catecholamines returned toward control levels in 3- to 4-day-SAD rats. These studies show that the chronic absence of arterial baroreceptor input produces time-related, regionally specific central changes of vasopressin and regionally associated catecholamines.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1999

Effects of adrenomedullin and PAMP on adrenal catecholamine release in dogs.

We examined the effects of proadrenomedullin-derived peptides on the release of adrenal catecholamines in response to cholinergic stimuli in pentobarbital sodium-anesthetized dogs. Drugs were administered into the adrenal gland through the phrenicoabdominal artery. Splanchnic nerve stimulation (1, 2, and 3 Hz) and ACh injection (0.75, 1.5, and 3 microgram) produced frequency- or dose-dependent increases in adrenal catecholamine output. These responses were unaffected by infusion of adrenomedullin (1, 3, and 10 ng. kg-1. min-1) or its selective antagonist adrenomedullin-(22-52) (5, 15, and 50 ng. kg-1. min-1). Proadrenomedullin NH2-terminal 20 peptide (PAMP; 5, 15, and 50 ng. kg-1. min-1) suppressed both the splanchnic nerve stimulation- and ACh-induced increases in catecholamine output in a dose-dependent manner. PAMP also suppressed the catecholamine release responses to the nicotinic agonist 1, 1-dimethyl-4-phenylpiperazinium (0.5, 1, and 2 microgram) and to muscarine (0.5, 1, and 2 microgram), although the muscarine-induced response was relatively resistant to PAMP. These results suggest that PAMP, but not adrenomedullin, can act as an inhibitory regulator of adrenal catecholamine release in vivo.

Acetylcholine↗
PubMed2000

Role of potassium channels in catecholamine secretion in the rat adrenal gland.

We elucidated the functional contribution of K(+) channels to cholinergic control of catecholamine secretion in the perfused rat adrenal gland. The small-conductance Ca(2+)-activated K(+) (SK(Ca))-channel blocker apamin (10-100 nM) enhanced the transmural electrical stimulation (ES; 1-10 Hz)- and 1, 1-dimethyl-4-phenyl-piperazinium (DMPP; 5-40 microM)-induced increases in norepinephrine (NE) output, whereas it did not affect the epinephrine (Epi) responses. Apamin enhanced the catecholamine responses induced by acetylcholine (6-200 microM) and methacholine (10-300 microM). The putative large-conductance Ca(2+)-activated K(+) channel blocker charybdotoxin (10-100 nM) enhanced the catecholamine responses induced by ES, but not the responses induced by cholinergic agonists. Neither the K(A) channel blocker mast cell degranulating peptide (100-1000 nM) nor the K(V) channel blocker margatoxin (10-100 nM) affected the catecholamine responses. These results suggest that SK(Ca) channels play an inhibitory role in adrenal catecholamine secretion mediated by muscarinic receptors and also in the nicotinic receptor-mediated secretion of NE, but not of Epi. Charybdotoxin-sensitive Ca(2+)-activated K(+) channels may control the secretion at the presynaptic site.

Acetylcholine↗
PubMed1988

Catecholamine and endorphin responses to delivery in term and preterm lambs.

A marked increase in catecholamines and endorphins at birth has been described in animals and man. Because the factors which regulate catecholamine secretion are incompletely understood and because it has been suggested that endogenous opiates are important in the regulation of catecholamine secretion, we designed studies to compare changes in plasma catecholamines at birth with simultaneously measured endorphins. Catecholamines and beta-endorphin-like immunoreactivity (beta-ELI) were measured at birth in term (145 days) and preterm (130 days) lambs. Preterm lambs were given natural sheep surfactant intratracheally to prevent respiration failure. Following umbilical cord cutting, there was a marked increase in circulating norepinephrine (NE) and epinephrine (E) levels. The peak preterm NE (2.2 +/- 0.3 ng/ml at 1 h) was greater than the peak term NE (1.0 +/- 0.2 ng/ml at 5 min). The peak preterm E occurred later and also was greater than the peak term E (4.0 +/- 0.5 ng/ml at 1 h vs. 1.3 +/- 0.4 ng/ml at 15 min, respectively, p less than 0.01). Baseline beta-ELI in term animals (767 +/- 15 pg/ml) was greater than preterm (456 +/- 12 pg/ml). Following cord cutting peak beta-ELI in term animals rose to 867 +/- 201 pg/ml compared to a peak beta-ELI in preterm animals of 1,866 +/- 450 pg/ml. These results and their significance for neonatal adaptation to extrauterine life are discussed.

Animals↗
PubMed2002

Angiotensin II induces catecholamine release by direct ganglionic excitation.

Angiotensin II (ANG) is known to facilitate catecholamine release from peripheral sympathetic neurons by enhancing depolarization-dependent exocytosis. In addition, a direct excitation by ANG of peripheral sympathetic nerve activity has recently been described. This study determined the significance of the latter mechanism for angiotensin-induced catecholamine release in the pithed rat. Rats were anesthetized and instrumented for measuring either hemodynamics and renal sympathetic nerve activity or plasma catecholamine concentrations in response to successively increasing doses of angiotensin infusions. Even during ganglionic blockade by hexamethonium (20 mg/kg), angiotensin dose-dependently elevated sympathetic nerve activity, whereas blood pressure-equivalent doses of phenylephrine were ineffective. Independently of central nervous sympathetic activity and ganglionic transmission, angiotensin (0.1 to 1 microg/kg) also induced an up-to 27-fold increase in plasma norepinephrine levels, reaching 2.65 ng/mL. Preganglionic electrical stimulation (0.5 Hz) raised basal norepinephrine levels 11-fold and further enhanced the angiotensin-induced increase in norepinephrine (4.04 ng/mL at 1 microg/kg ANG). Stimulation of sympathetic nerve activity and norepinephrine release were suppressed by candesartan (1 mg/kg) or tetrodotoxin (100 microg/kg), respectively. Angiotensin enhanced plasma norepinephrine, heart rate, and sympathetic nerve activity at similar threshold doses (0.3 to 1 microg/kg), but raised blood pressure at a significantly lower dose (0.01 microg/kg). It is concluded that direct stimulation of ganglionic angiotensin type 1 (AT(1)) receptors arouses electrical activity in sympathetic neurons, leading to exocytotic junctional catecholamine release. In both the absence and presence of preganglionic sympathetic activity, this mechanism contributes significantly to ANG-induced enhancement of catecholamine release.

Angiotensin II↗
PubMed1975

Diminished inotropic response of aged myocardium to catecholamines.

The effect of advanced age on the response of active tension, maximal rate of tension development (dT/dt), and contraction duration to catecholamines and to calcium was evaluated in isometric trabeculae carneae from young adult (6-month-old), middle-aged (12-month-old), and aged (25-month-old) rats. Control values were not age dependent except for that for contraction duration which was prolonged in the aged group. At a norepinephrine concentration of 8 times 10-5M, dT/dt increased to 163.8 plus or minus 5.3% of control in the young adult group and to 125.9 plus or minus 6.3% of control in the aged group (P smaller than 0.001). Active tension increased to 121.3 plus or minus 4.0% of control in the young adult muscles but did not increase in the aged muscles (P smaller than 0.01). Contraction duration shortened proportionately in both age groups. Similar results were obtained with isoproterenol. In contrast to the response to catecholamines, there was no age difference in the response of active tension and dT/dt to increasing concentrations of calcium. It is concluded that the intrinsic inotropic response to catecholamines is diminished in the aged myocardium. This finding does not appear to result from differences in tachyphylaxis, tissue uptake of catecholamines, or the ability of the contractile proteins to respond to increasing concentrations of calcium but instead may result from a decreased ability of catecholamines to increase the intracellular calcium available for contraction.

Aging↗
PubMed1999

Urinary catecholamine excretion in relation to renal function.

The urinary excretions of the free catecholamines noradrenaline, adrenaline and dopamine were measured in 50 patients (33 men and 17 women) with chronic renal failure. Stability studies showed that the catecholamines were stable in unacidified urine as long as the pH was not greater than 7.5 and the urine was acidified within 2-3 h of collection. The outputs of noradrenaline and dopamine correlated positively with creatinine clearance and in patients with clearances above 40 mL/min were similar to those in healthy volunteers (n = 20). However, adrenaline output was not correlated with creatinine clearance although it was lower in patients with renal failure compared with healthy volunteers. The urinary free catecholamine output during the first 10 days after a renal transplant was significantly less than normal, presumably because renal function was still impaired. However, in patients treated with cyclosporin A (CyA) combined with prednisolone the catecholamine excretion was lower compared with those treated with CyA and azathioprine. Impairment in renal function can have a marked effect on the output of free catecholamines and must be borne in mind when interpreting values that may have pathological significance.

Case-Control Studies↗