Lecture 19 - Hormones Of The Adrenal Cortex - Adrenal Gland

LECTURE 19: 11/3 Adrenal Gland C. Hormones of the adrenal cortex 4 Mineralcorticoid (mainly Aldosterone) a functions of aldosterone (hypertensive hormone)-1BP Distal Convoluted Tubule target of aldosterone -Na/K' exchange Na reabsorption (113 in blead) K'secretion (screted through urine) ~H₂O follows Na (Tretention of water volume b Regulation of aldosterone secretion. PRAS requires liver, kidney, langs not part of HRA Renin-Angiotensin System (RAS), 2. 2. increased [K"] in blood will adsterane Renin-Angiotensin System Step 1. Kidney releases renin dus to BP -enzyme Short 1/2 life in blood (15 min). Flenin Benin vetesse Mand pressure Na Start BP Step 2. liver secretes renin substrate (RS) Angiotensin I (A) 10 AA Angiotensinogen always present in blood Renin cleaves off decapeptide (10 A.A.) Livar Inactive peptide fragment RS Angiotensin-1 (A)-biologically inactive Renin Ponin substrate Step 3 Lung capillaries secrete a second enzyme -Angiotensin Converting Enzyme ACE-cuts 2AA from As fensive hermana! Angiotensin-I Angiotensin II (BA.A.1A How can Angstension A in hypertension raise BP? -TAVP retease from PN (Pars Nervаза) reabsorbs H₂O TBV TBP Hean methaniam A (8 AA) Hypothalamus Ag Brais purs nervosa PN AVP (+) - Idrinking water dispogenic response mechanism mechanism TBV TBP Drinking Induces Hugi sensation mechaniam -Tarteriale smooth muscle contraction -1 total peripheral resistance (TPR) increases blood pressure Increases TPR -Taldosterone secretion Summary of Ag in hypertension 1. TAVP release not mediated by A 2. Dispogenic 3. Presser effect (TPR) 4. Aldosterone Secretion net medistes by A Other actions of A -Tenzyme synthesis aminapeptidase a stimulates enzyme that will destroy self degrades Ag feedback -JG cells modified cells of the offent Kidney drop in blood pressure releases renin barowreceptors -Macula densa modified cells of the distal tubule -detects drops in Na (JG ceas releases remin cannot sense BP, anly [] in blaad if sensed parsering signats are sent to JG cetis chemoreceptors Renin- Angiotensin System BPar. No will activate JG cells to secrate reom remin encounters angetentinagen te suta 10A.A fragment te produce 1. Angiotensin 1 (A)-białegically inactive 2. inactive peptide fragment A. gats pumpes through heart, goes through pulmonary track le enter capillaries of the lungs. Here it will encounter ACE which chapa 24.A. from A, and il gets hurned into An Fig8-13 A (biologically active) travets trace heart to be pumped through the Bystemic syriem to reach all target fissues 1. Arienele smonth muscle It TPR, 187) 2. Thist region of brain (drinking, TBP) 3. Hypothalamus fars Nervosa mease of AVP (Twater retention. 18P) 4. Adrenal Cortex-Zone glomerulosa aldosterone secretion (TNa, TTBP) Ang- b. Regulation of aldosterone secretion 2 Actions of K high plasma [x] has direct effect on Zona glomerulasa increase aldosterone release increase Kexcretion primarily controlled through RAS not as sensitive to Angiotensin-III Atnzyme trantmembrane pen AAA. tates off one AA A repotensive formant Ang-clersinogen Corza-gafeway into body. ACE2 A1 ACE ACC NEP vasodilator ADE A- ACE Ang-1- (Ang antihypertrophic fights against aknermas enlargement of heart local control of vasodilation in Kidney, heart, smooth muacie a way of counteracting Ag (pertensive effects) Atrial Natriuretic Peptide-cas BP A. Source Function main source atrium of neart 1. induced by chronic high blood pressure 2. Protects against high BP Notriuretic? Na in urine-promotes excretion of Na" in urine B Targets for ANP Adrenal Cartes ANP inhibits aldosterone release reduces No reabsorption (LBP) 2. Brain ANP atrium AT BNP CNP brain esra is messere dameging effects of HBP marker for heate ANP inhibits AVP release causes diuresis (reduces retention of water. +BP) 3 Kidney ANP inhibits renin release couses diuresis LA ANP can directly inhiba aldosterone +AVP Ala LAVP Can also indirectly inhibit them by first inhibiting A. Tow water refention IV Clinical aspects of adrenal disorders A. GC hypersecretion 1. Cushing's Syndrome TGC umbrella of diseases have TGC (identifier) both Known unknown causes KNOWN-axa Cushing's Disease pituitary adenoma TACTH (not respoпането Feedback of GC) -adrenal hyperplasia, hypertrophy eie valed GCs (cannot have (-) feeabark) elevated adrenal androgens COUS Fnow F8-14