The adrenal medulla is essentially a component of the auto ). The principal hormone secreted by the adrenal medulla is epinephrine; some norepinephrine is also released. The rate of secretion of these catecholamines by the adrenal medulla is regulated by mechanisms that control the activity of the sympathetic nervous system. Concentrations of catecholamines in blood thus rise under the same conditions that activate the sympathetic nervous system. However, the cardiovascular effects of circulating catecholamines are probably minimal under normal conditions. Moreover, the pronounced changes in myocardial contractility with exercise, for example, are mediated mainly by the norepinephrine released from cardiac sympathetic nerve fibers rather than by the catecholamines released from the adrenal medulla.
How adrenocortical steroids influence myocardial contractility is controversial. Cardiac muscle taken from adrenalectomized animals and placed in a tissue bath is more likely to fatigue in response to stimulation than is cardiac muscle obtained from normal animals. In some species, however, adrenocortical hormones enhance contractility. In addition, the glucocorticoid hydrocortisone potentiates the cardiotonic effects of catecholamines. This potentiation is mediated in part by the ability of adrenocortical steroids to inhibit the extraneuronal catecholamine uptake mechanisms.
•Fig. 18.21 Vagus Nerve Stimulation Reduces Ventricular Con tractility. Pressure-volumecurvesobtainedatconstantventricular ratebeforeopenheartsurgeryinhuman.A, Controlpressure-volumecurveswerecalculatedduringocclusionoftheinferiorvenacava.Theend-systolicpressure-volumerelation,definedbytheslopeofthestraight line, measuredapproximately4mmHg/mL.B, Duringstimulationoftheleftvagusnerve,theslopeoftheend-systolicpressure-volumerelationdecreasedtoapproximately3mmHg/mL,anindicationthatcontractilityhaddecreased.LV,leftventricular.(RedrawnfromLewisME,Al-KhalidiAH,BonserRS,etal.Vagusnervestimulationdecreasesleftventricularcontractilityinvivointhehumanandpigheart.J Physiol. 2001;534:547.)
Thyroid hormones enhance myocardial contractility. Rates of ATP hydrolysis and Ca++ uptake by the sarcoplasmic reticulum are increased in hyperthyroidism; the opposite effects occur in hypothyroidism. Thyroid hormones increase cardiac protein synthesis, and this response leads to cardiac hypertrophy. These hormones also affect the composition of myosin isoenzymes in cardiac muscle. By increasing isoenzymes with the greatest ATPase activity, thyroid hormones enhance myocardial contractility.
Cardiovascularproblemsarecommoninpatientswithadrenocorticalinsufficiency(Addison’sdisease).Bloodvolume
The cardiovascular changes in thyroid dysfunction also depend on indirect mechanisms. Thyroid hyperactivity tendstofall,whichmayleadtoseverehypotensionandcardiovascularcollapse,theso-calledaddisoniancrisis(see