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,
1930S)

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 CUSHINGS
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
(CUSHINGS SYNDROME)
ANDROGEN: MASCULINIZATION,
PSEUDOHERMAPHODITISM,
PRECOCIOUS PSEUDOPUBERTY, NO
EFFECT IN ADULT MALES

ADRENAL INSUFFICIENY

CORTEX: ADDISONS 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