THE ADRENAL GLAND
D. C. MIKULECKY
PROFESSOR OF PHYSIOLOGY
AND
FACULTY MENTORING PROGRAM
THE ADRENAL GLANDS
CORTEX: STEROID HORMONES
SECRETED
MEDULLA: CATECHOLAMINES
(EPINEPHRIN AND NOREPINEPHRIN) SECRETED. IT IS A
MODIFIED SYMPATHETIC GANGLION
CORTEX: STEROID
HORMONES SECRETED
MINERALOCORTICOIDS
GLUCOCORTICOIDS
SEX HOMONES
STEROID HORMONES
CHOLESTEROL IS A COMMON
PRECURSOR
PREGNENOLONE IS A COMMON
INTERMEDIATE
DERIVATIVES OF THE POLYCYCLIC
PHENANTHRENE NUCLEUS
IMPORTANCE OF STEROID
HORMONES:
REMOVAL OF CORTEX LEADS TO
DEATH WITHIN 1 OR 2 WEEKS
WITHOUT REPLACEMENT THERAPY
EVERY ORGAN SYSTEM IS AFFECTED
MINERALOCORTICOIDS
 ALDOSTERONE
 ELECTROLYTE BALANCE
 BLOOD PRESSURE
 RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM
 ALDOSTERONE SECRETION REGULATED BY
RENIN SECRETION IN THE KIDNEY VIA
ANGIOTENSIN II
 NEGATIVE FEEDBACK CONTROL VIA
MONITORING BLOOD VOLUME
GLUCOCORTICOIDS
CORTISOL
GLOCONEOGENESIS
PERMISSIVE ACTIONS
STRESS ADAPTATION
ANTI-INFLAMITORY AND
IMMUNOSUPPRESSANT
SEE TABLE I IN TEXT
PERMISSIVE ACTION OF
CLUCOCORTICOIDS
STRESS INCREASES OUTPUT OF ACTH
FROM THE PITUITARY
THESE HORMONES SEEM TO GOVERN
PROCESSES FUNDAMENTAL TO NORMAL
FUNCTION IN MOST CELLS
TREATED AN ADRENALECTOMIZED
ANIMAL PERMITTED THE RESUMPTION OF
THESE FUNCTIONS (HANS SELYE, 1930’S)
EFFECTS OF GLUCOCORTICOIDS
ON ENERGY METABOLISM
MAINTAIN CARBOHYDRATE RESERVES
HYPOGLYCEMIA IF ABSENT
GLUCONEOGENESIS: DIRECT EFFECTS
AND INCREASES IN ENZYMES
DECREASE UTILIZATION OF GLUCOSE BY
MUSCLE AND ADIPOSE TISSUE AND
LOWER SENSITIVITY TO INSULIN.
DIABETES MAY ACCOMPANY CUSHING’S
DISEASE WHICH IS A HYPERSECRETION
ANTI-INFLAMITORY EFFECTS
OF GLUCOCORTICOIDS
INFLUENCE ON PROSTAGLANDINS:
SUPPRESS SYNTHESIS OF CYCLOOXYGENASE
POSSIBLY INHIBIT HISTAMINE
FORMATION
CYTOKINES (INTERLEUKIN-1)
GLUCOCORTICOIDS AND THE
IMMUNE RESPONSE
BLOCK CYTOKINE PRODUCTION
MAY ALSO KILL T-CELLS
REGULATION OF CORTISOL
SECRETION
HYPOTHALAMUS
STRESS
+
CRH
+
-
DIURNAL
RHYTHM
ANTERIOR PITUITARY
INCREASED
BLOOD GLUCOSE
BLOOD AA
BLOOD FATTY ACIDS
ACTH
-
ADRENAL CORTEX
CORTISOL
TARGET ORGANS
ACTION OF ACTH
STIMULATES STEROIDOGENESIS
INCREASES STEROID SECRETION
WITHIN 1 TO 2 MINUTES
PEAK RATES IN ABOUT 15 MINUTES
cAMP ---> PROTEIN KINASE A
ABSENCE LEADS TO ATROPHY OF
INNER ZONES OF ADRENAL CORTEX
SEX HOMONES
ANDROGENS (TESTOSTERONE)
ESTROGENS
LESS THAN GONADS
ADRENAL STEROID
HORMONES IN THE BLOOD
BOUND TO TRANSCORTIN OR
CORTICOSTEROID BINDING GLOBULIN
(CBG)
SECRETED BY LIVER BUT AT 1/1000 TH
THE CONCENTRATION OF ALBUMIN
95% CLUCOCORTICOIDS AND 65%
ALDOSTERONE
LONG HALF LIFE (90 AND 30 MINUTES)
METABOLISM AND EXCRETION OF
ADRENAL CORTICAL HORMONES
INACTIVATION MAINLY IN LIVER
MAKES THEM UNRECONIZABLE TO
RECEPTORS
EXCRETED IN URINE
ADRENAL
OVERSECRETION
MINERALCORTICOIDS: SODIUM
RETENTION, POTASSIUM DEPLETION
CORTISOL:EXCESS GLUCONEOGENESISEXCESS GLUCOSE DEPOSITED AS FAT
(CUSHING’S SYNDROME)
ANDROGEN: MASCULINIZATION,
PSEUDOHERMAPHODITISM, PRECOCIOUS
PSEUDOPUBERTY, NO EFFECT IN ADULT
MALES
ADRENAL INSUFFICIENY
CORTEX: ADDISON’S DISEASE
POOR RESPONSE TO STRESS
LACK OF PERMISSIVE ACTION
POTASSIUM RETENTION
HYPOTENSION
MEDULLA: CATECHOLAMINES
A MODIFIED SYMPATHETIC POST
GANGLIONIC NEURON
EPINEPHRINE
ACTIONS OF EPINEPHRINE
MIMICS SYMPATHETIC NS
MOBILIZES STORED FAT AND
CARBOHYDRATE
HEART AND BLOOD VESSELS
GENERAL ADAPTATION
SYNDROME
FLIGHT OR FIGHT
EPINEPHRINE
CRH-ACTH-CORTISOL
RENIN-ANGIOTENSIN-ALDOSTERONE
VASOPRESSIN
COORDINATED BY HYPOTHALAMUS
CAN BE INDUCED PSYCHOSOCIALLY
EPINEPHRINE, CORTISOL, AND
GROWTH HORMONE
ALL INCREASE BLOOD GLUCOSE AND
FATTY ACIDS
CORTISOL INCREASES BLOOD AA
AND DECREASES MUSCLE PROTEIN
GH DECREASES BLOOD AA AND
INCREASES MUSCLE PROTEIN