The adrenal medulla, an integral part of the autonomic nervous system, primarily secretes epinephrine and some norepinephrine. The release of these catecholamines is regulated by the sympathetic nervous system. Their levels in the blood increase under conditions that activate the sympathetic nervous system. However, the impact of circulating catecholamines on cardiovascular function is likely minimal under normal circumstances. The significant changes in myocardial contractility during exercise, for example, are mainly mediated by norepinephrine released from cardiac sympathetic nerve fibers rather than catecholamines from the adrenal medulla.

The influence of adrenocortical steroids on myocardial contractility is a subject of debate. Cardiac muscle obtained from adrenalectomized animals tends to fatigue more readily when stimulated compared to muscle from normal animals. However, in some species, adrenocortical hormones enhance contractility. Additionally, the glucocorticoid hydrocortisone enhances the cardiotonic effects of catecholamines by inhibiting extraneuronal catecholamine uptake mechanisms.

Thyroid hormones have a positive impact on myocardial contractility. In hyperthyroidism, rates of ATP hydrolysis and Ca++ uptake by the sarcoplasmic reticulum increase, while the opposite occurs in hypothyroidism. Thyroid hormones promote cardiac protein synthesis, leading to cardiac hypertrophy. They also influence the composition of myosin isoenzymes in cardiac muscle, enhancing contractility by increasing isoenzymes with greater ATPase activity.

Patients with adrenocortical insufficiency (Addison's disease) commonly experience cardiovascular problems. Thyroid dysfunction can also contribute to cardiovascular changes through indirect mechanisms. Excessive thyroid activity can cause a decrease in blood volume, potentially leading to severe hypotension and cardiovascular collapse, known as an addisonian crisis.
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